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Journal articles on the topic 'Atherosclerosis'
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1
Napieralski, Rudolf, Ernst Wagner, Harry Gebhard, Manfred Schmitt, Alexander Zimmermann, Hans-Henning Eckstein, Anna Greißel, Mihaela Culmes, Alma Zernecke, and Jaroslav Pelisek. "Alternation of histone and DNA methylation in human atherosclerotic carotid plaques." Thrombosis and Haemostasis 114, no. 08 (2015): 390–402. http://dx.doi.org/10.1160/th14-10-0852.
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SummaryLittle is known about epigenetics and its possible role in atherosclerosis. We here analysed histone and DNA methylation and the expression of corresponding methyltransferases in early and advanced human atherosclerotic carotid lesions in comparison to healthy carotid arteries. Western Blotting was performed on carotid plaques from our biobank with early (n=60) or advanced (n=60) stages of atherosclerosis and healthy carotid arteries (n=12) to analyse di-methylation patterns of histone H3 at positions K4, K9 and K27. In atherosclerotic lesions, di-methylation of H3K4 was unaltered and that of H3K9 and H3K27 significantly decreased compared to control arteries. Immunohistochemistry revealed an increased appearance of di-methylated H3K4 in smooth muscle cells (SMCs), a decreased expression of di-methylated H3K9 in SMCs and inflammatory cells, and reduced di-methylated H3K27 in inflammatory cells in advanced versus early atherosclerosis. Expression of corresponding histone methyltransferases MLL2 and G9a was increased in advanced versus early atherosclerosis. Genomic DNA hypomethylation, as determined by PCR for methylated LINE1 and SAT-alpha, was observed in early and advanced plaques compared to control arteries and in cell-free serum of patients with high-grade carotid stenosis compared to healthy volunteers. In contrast, no differences in DNA methylation were observed in blood cells. Expression of DNA-methyltransferase DNMT1 was reduced in atherosclerotic plaques versus controls, DNMT3A was undetectable, and DNMT3B not altered. DNA-demethylase TET1 was increased in atherosclerosisc plaques. The extent of histone and DNA methylation and expression of some corresponding methyltransferases are significantly altered in atherosclerosis, suggesting a possible contribution of epigenetics in disease development.
2
Li, Junxi, Xinying Fu, Renyi Yang, and Wei Zhang. "Atherosclerosis Vascular Endothelial Secretion Dysfunction and Smooth Muscle Cell Proliferation." Journal of Healthcare Engineering 2022 (March 9, 2022): 1–13. http://dx.doi.org/10.1155/2022/9271879.
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Atherosclerosis is a chronic inflammatory disease of the arterial wall and the main cause of cardiovascular disease and cerebrovascular disease. In recent years, the mortality rate of atherosclerotic diseases has become higher and higher. This article aims to study the dysregulation of atherosclerotic vascular endothelial secretion and smooth muscle cell proliferation, and put forward and practice the pathological research of atherosclerotic disease. This article describes in detail atherosclerosis, endothelial dysfunction, and smooth muscle cell proliferation, and studies the causes of atherosclerosis. Research results indicate that atherosclerotic vascular endothelial dysfunction also has a great influence on the proliferation of smooth muscle cells. Many genes and environmental factors can regulate the functions of endothelial cells, vascular smooth muscle cells, and mononuclear macrophages and affect the formation of atherosclerosis. At the same time, diabetes, hypertension, hyperlipidemia, obesity, etc. are the main causes of atherosclerosis. The number of patients with cardiovascular and cerebrovascular diseases dying from atherosclerosis in the country is increasing, and the proportion is close to 30%.
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Xia, Mingcan, Kangkang Yang, Nadia Guerra, Glina Sukhova, Carla Miller, Guo-Ping Shi, David Raulet, and Na Xiong. "NKG2D/ligands-mediated immune activation promotes atherosclerosis (142.7)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 142.7. http://dx.doi.org/10.4049/jimmunol.184.supp.142.7.
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Abstract Atherosclerosis, a chronic vascular disease, is characterized by deposition of fatty substances and accumulation of immune cells in susceptible regions of arteries. Increasing evidence show that abnormal metabolic conditions, such as dyslipdemia and diabetes, induce immune cell activation and inflammation, which play crucial roles in progression of atherosclerosis. However, molecular linkers of metabolic disorder, immune activation and atherosclerosis are not well understood. Here we report that ligands for NKG2D, an immune-activating receptor, were upregulated in multiple tissues and organs under atherosclerotic disease condition, particularly in atherosclerotic lesion and liver. Preventing NKG2D/ligands interaction significantly reduced atherosclerotic lesion formation and systemic inflammation. In addition, preventing NKG2D/ligand interaction alleviated abnormal metabolic conditions by suppressing liver inflammation. Our data clearly show that NKG2D/ligand interaction plays critical roles in the progression of atherosclerosis and might be potential targets against atherosclerosis.
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Konstantinova, E. V., A. A. Bogdanova, A. A. Sagatelyan, A. I. Kovaikin, E. S. Pershina, and M. Yu Gilyarov. "Features of atherosclerosis in carotid and coronary arteries." Meditsinskiy sovet = Medical Council, no. 14 (October 18, 2021): 44–53. http://dx.doi.org/10.21518/2079-701x-2021-14-44-53.
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Atherothrombosis is a leading cause of myocardial infarction and ischemic atherothrombotic stroke. It represents a stage of atherosclerosis which is a pathologic process throughout the circulatory system. However, atherosclerosis has specific development characteristics in different vascular beds. Multiple factors contribute to atherosclerosis formation and progression such as genetic factors, vessel hemodynamics, and vessel anatomy. A better understanding of differences in vessels would improve prevention and treatment of atherosclerosis and its complication. In this article we review features of atherosclerosis in carotid and coronary vessels. We discuss specific conditions of local hemodynamics in the areas of bifurcation which promote atherosclerotic plaque progression, and review characteristics of unstable plaques in carotid and coronary vessels. We analyze immunologic and inflammatory processes, extracellular matrix degradation and remodeling, cellular apoptosis and autophagy occurring during atherosclerotic plaque destabilization as well as the possibility of diffuse plaque instability in systemic atherosclerosis. We review association and interaction of atherosclerotic processes in coronary and carotid arteries, and its significance for a patient. Improvement in understanding of atherosclerosis pathogenesis can lead to advances in atherosclerosis prevention. Timely and effective interventions would promote prevention of myocardial infarction and ischemic stroke which is highly important taking into account high mortality and morbidity rates.
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Pakzad, Bahram, Elham Rajae, Saeid Shahrabi, Somayeh Mansournezhad, Nader Davari, Shirin Azizidoost, and Najmaldin Saki. "T-Cell Molecular Modulation Responses in Atherosclerosis Anergy." Laboratory Medicine 51, no. 6 (February 27, 2020): 557–65. http://dx.doi.org/10.1093/labmed/lmaa003.
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Abstract Atherosclerosis continues to be a major cause of death in patients with cardiovascular diseases. The cooperative role of immunity has been recently considered in atherosclerotic plaque inflammation, especially adaptive immune response by T cells. In this review, we examine the possible role of T cells in atherosclerosis-mediated inflammation and conceivable therapeutic strategies that can ameliorate complications of atherosclerosis. The cytokines secreted by T-lymphocyte subsets, different pathophysiological profiles of microRNAs (miRs), and the growth factor/receptor axis have diverse effects on the inflammatory cycle of atherosclerosis. Manipulation of miRNA expression and prominent growth factor receptors involved in inflammatory cytokine secretion in atherosclerosis can be considered diagnostic biomarkers in the induction of anergy and blockade of atherosclerotic development. This manuscript reviews immunomodulation of T cells responses in atherosclerosis anergy.
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Li, Yang, Yi Feng, Genshan Ma, Chengxing Shen, and Naifeng Liu. "Coronary tortuosity is negatively correlated with coronary atherosclerosis." Journal of International Medical Research 46, no. 12 (October 10, 2018): 5205–9. http://dx.doi.org/10.1177/0300060518804723.
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Objective The impact of coronary tortuosity on coronary atherosclerosis remains unclear. This study was performed to determine to the relationship between coronary tortuosity and the presence of coronary atherosclerosis. Methods Tortuosity and the presence of coronary atherosclerosis in the main coronary arteries were evaluated. The coronary artery was divided into non-tortuous and tortuous segments. The incidence of coronary atherosclerosis between the two segments was compared. Results The prevalence of coronary atherosclerotic stenosis was significantly lower in the tortuous than non-tortuous segment. Conclusion The prevalence of coronary atherosclerotic stenosis is lower in the coronary tortuous than non-tortuous segment, indicating that coronary tortuosity might be considered a protective factor for atherosclerosis.
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Yang, Yang, Lixia Yang, Xing Liang, and Guofu Zhu. "MicroRNA-155 Promotes Atherosclerosis Inflammation via Targeting SOCS1." Cellular Physiology and Biochemistry 36, no. 4 (2015): 1371–81. http://dx.doi.org/10.1159/000430303.
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Aims: Accumulating evidence suggests that atherosclerotic progression depends on persistent and chronic inflammation in the arterial walls. MicroRNA-155 is reportedly involved in cardiovascular disease and has been implicated as a pro-inflammation regulator. Although some researchers have focused on microRNA-155 as an atherosclerosis regulator, the mechanisms by which microRNA-155 functions as a putative pro-atherosclerosis microRNA are largely unknown. This study aims to analyze microRNA-155's effects on atherosclerotic inflammation and to explore its mechanism. Methods: MicroRNA-155's effects on atherosclerotic inflammation were observed along with the expression and activity levels of SOCS1, STAT3 and NF-κB though microRNA-155 inhibition or overexpression. Results: Highly expressions of microRNA-155 in oxLDL-stimulated macrophages and atherosclerosis mice were inversely correlated with SOCS1 expression. Ectopic microRNA-155 overexpression significantly promoted inflammatory cytokine and chemokine production and atherosclerosis progression. We then observed microRNA-155's functional role in the atherosclerotic pathophysiological process in vivo and in vitro. The observation revealed that by enhancing STAT3 and NF-κB signaling and facilitating immune inflammation by targeting SOCS1, microRNA-155 plays a promotable role in atherosclerosis progression. Conclusions: microRNA-155 works as a promoter in the atherosclerotic procession. Its mechanism may include enhancing inflammatory response in atherosclerosis by increasing STAT3 and NF-κB signaling via targeting SOCS1.
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Kozhanova, T. V., E. V. Neudakhin, S. S. Zhilina, T. I. Mescheryakova, A. A. Abramov, E. N. Lukash, and A. G. Prityko. "THE GENETIC SUSCEPTIBILITY TO ATHEROSCLEROSIS." Russian Archives of Internal Medicine 8, no. 6 (December 3, 2018): 407–17. http://dx.doi.org/10.20514/2226-67042018-8-6-407-417.
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Atherosclerosis is a complex multifocal arterial disease involving interactions of multiple genetic and environmental factors. Atherosclerosis is the main cause of death and disability in developed countries, while in developing countries the incidence of this pathology is growing rapidly. Advances in techniques of molecular genetics have revealed that genetic polymorphisms significantly influence susceptibility to atherosclerotic vascular diseases. A large number of candidate genes, genetic polymorphisms and susceptibility loci associated with atherosclerotic diseases have been identified in recent years and their number is rapidly increasing. In recent years, there is significant interest in identifying additional factors of genetic risk for atherosclerosis. In recent years, a large number of genetic studies have been carried out to prove the genetic effect on the atherosclerotic process. Rapid progress in the sequencing of the human genome and molecular genetic methods have helped in the definition of susceptibility loci and associated candidate genes with atherosclerosis and concomitant diseases. The association of a large number of susceptibility genes with atherosclerosis reflects the enormous complexity of the disease. Multiple factors, including endothelial dysfunction, lipid metabolism defects, inflammation and immune responses, oxidative stress, cell proliferation, tissue remodeling and hemostatic defects are involved in the pathogenesis of atherosclerosis. In this review we focus and discuss on some of the major candidate genes and genetic polymorphisms associated with human atherosclerotic vascular diseases.
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Raman Parajuli, Sudhir, Bishwonath Yadav, Prahlad Karki, Paricha Upadhyaya, and Shivendra Jha. "An Autopsy Study of Atherosclerotic Changes in Coronary Arteries at B.P. Koirala Institute of Health Sciences." Annapurna Journal of Health Sciences 1, no. 1 (February 10, 2021): 4–8. http://dx.doi.org/10.52910/ajhs.5.
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Introduction: Atherosclerosis is a giant killer and the incidence of atherosclerosis in coronary arteries is rapidly increasing. The study was designed to assess the atherosclerotic lesions in coronary artery and to correlate the risk factors related to prevalence of atherosclerosis.
Methods: Heart from 100 medico legal autopsy cases ranging between ages 15 to 35 years which came to BPKIHS Dharan were taken for this study and processed for coronary arteries using conventional technique. They were then studied,and grading was done based on Modified American Heart Association (AHA) classification of atherosclerosis.
Results: Intimal thickening was noted in more than 90% in all three coronary arteries followed by intimal xanthoma whereas intermediate lesion for atherosclerosis was not found. Age, gender, smoking and alcohol in relation to atherosclerosis were found to be of no significance.
Conclusion: The study highlights the impact of atherosclerotic lesions in the Eastern region of Nepal. Meticulous postmortem examination along with histopathological study is the best possible way to study atherosclerotic disease in humans and risk factors associated with it.
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Iannuzzi, Arcangelo, Paolo Rubba, Marco Gentile, Vania Mallardo, Ilenia Calcaterra, Alessandro Bresciani, Giuseppe Covetti, et al. "Carotid Atherosclerosis, Ultrasound and Lipoproteins." Biomedicines 9, no. 5 (May 6, 2021): 521. http://dx.doi.org/10.3390/biomedicines9050521.
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Carotid artery plaques are considered a measure of atherosclerosis and are associated with an increased risk of atherosclerotic cardiovascular disease, particularly ischemic strokes. Monitoring of patients with an elevated risk of stroke is critical in developing better prevention strategies. Non-invasive imaging allows us to directly see atherosclerosis in vessels and many features that are related to plaque vulnerability. A large body of evidence has demonstrated a strong correlation between some lipid parameters and carotid atherosclerosis. In this article, we review the relationship between lipids and atherosclerosis with a focus on carotid ultrasound, the most common method to estimate atherosclerotic load.
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Peycheva, Marieta, Tanya Deneva, Dora Zlatareva, Tina Zdravkova, Lubomir Chervenkov, and Zdrvaka Harizanova. "Image and Laboratory Aspects of Carotid Atherosclerosis." Experimental and Applied Biomedical Research (EABR) 24, no. 2 (June 1, 2023): 135–44. http://dx.doi.org/10.2478/sjecr-2022-0047.
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Abstract Carotid atherosclerosis is a main risk factor for ischemic stroke. Plaque instability is determined by the morphological characteristics of the plaque and can be characterized by immunological biomarkers. The study aimed to examine the connection between serum levels of hs-CRP, fibrinogen, ICAM-1, VCAM-1 and carotid atherosclerosis and the different types of atherosclerotic plaques imaged by ultrasound and magnetic resonance. The study involved 120 patients with carotid atherosclerosis and 33 patients without carotid atherosclerosis. Blood samples were collected to analyze the serum level of hs-CRP, fibrinogen, ICAM-1 and VCAM-1. The ultrasound analysis included detection of atherosclerotic plaques in the internal carotid arteries, measurement of artery stenosis in percentage and determination of plaque types by the classification of Gray-Weales/Gerolacus. A small subset of 30 patients with carotid atherosclerosis performed 3T magnetic resonance imaging. Atherosclerotic plaques were classified into 8 types based on the modified MR classification of the American Heart Association. Significantly higher serum levels of hs-CRP (p <0.001) and fibrinogen (p = 0.018) were observed in patients with carotid atherosclerosis compared to patients without atherosclerosis. Criterion values for hs-CRP > 4.13mg/l and for fibrinogen > 3.6 g/l were associated with the presence of carotid plaques with accuracy of 70%. No relation was observed between the investigated biomarkers, the artery stenosis and the types of atherosclerotic plaques determined by ultrasound and magnetic resonance diagnostic methods. Hs-CRP and fibrinogen are reliable serum markers whose increased serum concentrations are connected with the presence of carotid atherosclerosis.
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Henein, Michael Y., Sergio Vancheri, Gani Bajraktari, and Federico Vancheri. "Coronary Atherosclerosis Imaging." Diagnostics 10, no. 2 (January 24, 2020): 65. http://dx.doi.org/10.3390/diagnostics10020065.
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Identifying patients at increased risk of coronary artery disease, before the atherosclerotic complications become clinically evident, is the aim of cardiovascular prevention. Imaging techniques provide direct assessment of coronary atherosclerotic burden and pathological characteristics of atherosclerotic lesions which may predict the progression of disease. Atherosclerosis imaging has been traditionally based on the evaluation of coronary luminal narrowing and stenosis. However, the degree of arterial obstruction is a poor predictor of subsequent acute events. More recent techniques focus on the high-resolution visualization of the arterial wall and the coronary plaques. Most acute coronary events are triggered by plaque rupture or erosion. Hence, atherosclerotic plaque imaging has generally focused on the detection of vulnerable plaque prone to rupture. However, atherosclerosis is a dynamic process and the plaque morphology and composition may change over time. Most vulnerable plaques undergo progressive transformation from high-risk to more stable and heavily calcified lesions, while others undergo subclinical rupture and healing. Although extensive plaque calcification is often associated with stable atherosclerosis, the extent of coronary artery calcification strongly correlates with the degree of atherosclerosis and with the rate of future cardiac events. Inflammation has a central role in atherogenesis, from plaque formation to rupture, hence in the development of acute coronary events. Morphologic plaque assessment, both invasive and non-invasive, gives limited information as to the current activity of the atherosclerotic disease. The addition of nuclear imaging, based on radioactive tracers targeted to the inflammatory components of the plaques, provides a highly sensitive assessment of coronary disease activity, thus distinguishing those patients who have stable disease from those with active plaque inflammation.
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Tanaka, Toru, Naoto Sasaki, and Yoshiyuki Rikitake. "Recent Advances on the Role and Therapeutic Potential of Regulatory T Cells in Atherosclerosis." Journal of Clinical Medicine 10, no. 24 (December 16, 2021): 5907. http://dx.doi.org/10.3390/jcm10245907.
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Atherosclerotic diseases, including ischemic heart disease and stroke, are a main cause of mortality worldwide. Chronic vascular inflammation via immune dysregulation is critically involved in the pathogenesis of atherosclerosis. Accumulating evidence suggests that regulatory T cells (Tregs), responsible for maintaining immunological tolerance and suppressing excessive immune responses, play an important role in preventing the development and progression of atherosclerosis through the regulation of pathogenic immunoinflammatory responses. Several strategies to prevent and treat atherosclerosis through the promotion of regulatory immune responses have been developed, and could be clinically applied for the treatment of atherosclerotic cardiovascular disease. In this review, we summarize recent advances in our understanding of the protective role of Tregs in atherosclerosis and discuss attractive approaches to treat atherosclerotic disease by augmenting regulatory immune responses.
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Zhou, Zhi-Xiang, Zhong Ren, Bin-Jie Yan, Shun-Lin Qu, Zhi-Han Tang, Dang-Heng Wei, Lu-Shan Liu, Min-Gui Fu, and Zhi-Sheng Jiang. "The Role of Ubiquitin E3 Ligase in Atherosclerosis." Current Medicinal Chemistry 28, no. 1 (December 29, 2020): 152–68. http://dx.doi.org/10.2174/0929867327666200306124418.
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: Atherosclerosis is a chronic inflammatory vascular disease. Atherosclerotic cardiovascular disease is the main cause of death in both developed and developing countries. Many pathophysiological factors, including abnormal cholesterol metabolism, vascular inflammatory response, endothelial dysfunction and vascular smooth muscle cell proliferation and apoptosis, contribute to the development of atherosclerosis and the molecular mechanisms underlying the development of atherosclerosis are not fully understood. Ubiquitination is a multistep post-translational protein modification that participates in many important cellular processes. Emerging evidence suggests that ubiquitination plays important roles in the pathogenesis of atherosclerosis in many ways, including regulation of vascular inflammation, endothelial cell and vascular smooth muscle cell function, lipid metabolism and atherosclerotic plaque stability. This review summarizes important contributions of various E3 ligases to the development of atherosclerosis. Targeting ubiquitin E3 ligases may provide a novel strategy for the prevention of the progression of atherosclerosis.
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Piollet, Marie, Florentina Porsch, Giuseppe Rizzo, Frederieke Kapser, Dirk J. J. Schulz, Máté G. Kiss, Kai Schlepckow, et al. "TREM2 protects from atherosclerosis by limiting necrotic core formation." Nature Cardiovascular Research 3, no. 3 (March 12, 2024): 269–82. http://dx.doi.org/10.1038/s44161-024-00429-9.
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AbstractAtherosclerosis is a chronic disease of the vascular wall driven by lipid accumulation and inflammation in the intimal layer of arteries, and its main complications—myocardial infarction and stroke—are the leading cause of mortality worldwide1,2. Recent studies have identified triggering receptor expressed on myeloid cells 2 (TREM2), a lipid-sensing receptor regulating myeloid cell functions3, to be highly expressed in macrophage foam cells in experimental and human atherosclerosis4. However, the role of TREM2 in atherosclerosis is not fully known. Here we show that hematopoietic or global TREM2 deficiency increased, whereas TREM2 agonism decreased, necrotic core formation in early atherosclerosis. We demonstrate that TREM2 is essential for the efferocytosis capacities of macrophages and to the survival of lipid-laden macrophages, indicating a crucial role of TREM2 in maintaining the balance between foam cell death and clearance of dead cells in atherosclerotic lesions, thereby controlling plaque necrosis.
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Schäfer, Sarah, and Alma Zernecke. "CD8+ T Cells in Atherosclerosis." Cells 10, no. 1 (December 29, 2020): 37. http://dx.doi.org/10.3390/cells10010037.
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Atherosclerotic lesions are populated by cells of the innate and adaptive immune system, including CD8+ T cells. The CD8+ T cell infiltrate has recently been characterized in mouse and human atherosclerosis and revealed activated, cytotoxic, and possibly dysfunctional and exhausted cell phenotypes. In mouse models of atherosclerosis, antibody-mediated depletion of CD8+ T cells ameliorates atherosclerosis. CD8+ T cells control monopoiesis and macrophage accumulation in early atherosclerosis. In addition, CD8+ T cells exert cytotoxic functions in atherosclerotic plaques and contribute to macrophage cell death and necrotic core formation. CD8+ T cell activation may be antigen-specific, and epitopes of atherosclerosis-relevant antigens may be targets of CD8+ T cells and their cytotoxic activity. CD8+ T cell functions are tightly controlled by costimulatory and coinhibitory immune checkpoints. Subsets of regulatory CD25+CD8+ T cells with immunosuppressive functions can inhibit atherosclerosis. Importantly, local cytotoxic CD8+ T cell responses may trigger endothelial damage and plaque erosion in acute coronary syndromes. Understanding the complex role of CD8+ T cells in atherosclerosis may pave the way for defining novel treatment approaches in atherosclerosis. In this review article, we discuss these aspects, highlighting the emerging and critical role of CD8+ T cells in atherosclerosis.
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Jednacz, Ewa, and Lidia Rutkowska-Sak. "Atherosclerosis in Juvenile Idiopathic Arthritis." Mediators of Inflammation 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/714732.
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Atherosclerosis is a chronic inflammatory disease of the arteries. Clinical consequences of the atherosclerotic process occur in the adult population, however atherosclerotic process begins in childhood. The classic risk factors for atherosclerosis include obesity, dyslipidaemia, age, gender or family history. In recent years, attention has been drawn to the similarity between atherosclerotic inflammatory processes and inflammatory changes in the course of systemic connective tissue disease, in particular systemic lupus etythematosus (SLE) or rheumatoid arthritis (RA). There is also observed the similarity of the pathogenetic background of development of atherosclerosis and juvenile idiopathic arthritis (JIA). Elevated levels of pro-inflammatory cytokines are observed in the course of juvenile idiopathic arthritis. Also homocysteine concentrations, which may play a significant role in the development of atherosclerotic lesions, are observed higher in patients with JIA. Some studies revealed higher carotid intima-media thickness (IMT) index values in children with JIA. In view of the fact that atherosclerotic process begins as early as in childhood, the introduction of appropriate preventive measures in children is a matter of utmost importance.
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Hartman, Robin J. G., Katie Owsiany, Lijiang Ma, Simon Koplev, Ke Hao, Lotte Slenders, Mete Civelek, et al. "Sex-Stratified Gene Regulatory Networks Reveal Female Key Driver Genes of Atherosclerosis Involved in Smooth Muscle Cell Phenotype Switching." Circulation 143, no. 7 (February 16, 2021): 713–26. http://dx.doi.org/10.1161/circulationaha.120.051231.
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Background: Although sex differences in coronary artery disease are widely accepted with women developing more stable atherosclerosis than men, the underlying pathobiology of such differences remains largely unknown. In coronary artery disease, recent integrative systems biological studies have inferred gene regulatory networks (GRNs). Within these GRNs, key driver genes have shown great promise but have thus far been unidentified in women. Methods: We generated sex-specific GRNs of the atherosclerotic arterial wall in 160 women and age-matched men in the STARNET study (Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task). We integrated the female GRNs with single-cell RNA-sequencing data of the human atherosclerotic plaque and single-cell RNA sequencing of advanced atherosclerotic lesions from wild type and Klf4 knockout atherosclerotic smooth muscle cell (SMC) lineage-tracing mice. Results: By comparing sex-specific GRNs, we observed clear sex differences in network activity within the atherosclerotic tissues. Genes more active in women were associated with mesenchymal cells and endothelial cells, whereas genes more active in men were associated with the immune system. We determined that key drivers of GRNs active in female coronary artery disease were predominantly found in (SMCs by single-cell sequencing of the human atherosclerotic plaques, and higher expressed in female plaque SMCs, as well. To study the functions of these female SMC key drivers in atherosclerosis, we examined single-cell RNA sequencing of advanced atherosclerotic lesions from wild type and Klf4 knockout atherosclerotic SMC lineage-tracing mice. The female key drivers were found to be expressed by phenotypically modulated SMCs and affected by Klf4, suggesting that sex differences in atherosclerosis involve phenotypic switching of plaque SMCs. Conclusions: Our systems approach provides novel insights into molecular mechanisms that underlie sex differences in atherosclerosis. To discover sex-specific therapeutic targets for atherosclerosis, an increased emphasis on sex-stratified approaches in the analysis of multi-omics data sets is warranted.
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Yu, Qun, Yilin Zhang, Wenyun Zeng, Yingxin Sun, Xiaolu Zhang, Lin Guo, Yue Zhang, et al. "Buyang Huanwu Decoction Alleviates Atherosclerosis by Regulating gut Microbiome and Metabolites in Apolipoprotein E-deficient Mice fed with High-fat Diet." Chinese Journal of Physiology 67, no. 2 (March 2024): 88–102. http://dx.doi.org/10.4103/ejpi.ejpi-d-23-00031.
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Abstract The traditional Chinese herbal prescription Buyang Huanwu decoction (BHD), effectively treats atherosclerosis. However, the mechanism of BHD in atherosclerosis remains unclear. We aimed to determine whether BHD could alleviate atherosclerosis by altering the microbiome-associated metabolic changes in atherosclerotic mice. An atherosclerotic model was established in apolipoprotein E-deficient mice fed high-fat diet, and BHD was administered through gavage for 12 weeks at 8.4 g/kg/d and 16.8 g/kg/d. The atherosclerotic plaque size, composition, serum lipid profile, and inflammatory cytokines, were assessed. Mechanistically, metabolomic and microbiota profiles were analyzed by liquid chromatography-mass spectrometry and 16S rRNA gene sequencing, respectively. Furthermore, intestinal microbiota and atherosclerosis-related metabolic parameters were correlated using Spearman analysis. Atherosclerotic mice treated with BHD exhibited reduced plaque area, aortic lumen occlusion, and lipid accumulation in the aortic root. Nine perturbed serum metabolites were significantly restored along with the relative abundance of microbiota at the family and genus levels but not at the phylum level. Gut microbiome improvement was strongly negatively correlated with improved metabolite levels. BHD treatment effectively slows the progression of atherosclerosis by regulating altered intestinal microbiota and perturbed metabolites.
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Nehler, M. R., L. M. Taylor, and J. M. Porter. "Homocysteinemia as a Risk Factor for Atherosclerosis: A Review." Cardiovascular Surgery 5, no. 6 (December 1997): 559–67. http://dx.doi.org/10.1177/096721099700500603.
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In industrialized nations, the leading cause of death and disability is atherosclerosis. Despite a widespread research effort spanning decades, there remains no clearly defined cause or cure for this disease that directly or indirectly affects the lives of almost all individuals in the western world. Autopsy findings show atherosclerosis to some degree in nearly all aged people, suggesting it should be regarded as a normal aging process as well as a disease. Any investigation of atherosclerosis etiology therefore requires a distinction between atherosclerosis normally observed with aging, and pathologic atherosclerosis causing disease and/or death. Atherosclerosis is most appropriately regarded as a disease when associated with both rapid progression and clinical symptoms. Widely accepted risk factors for atherosclerotic disease include advanced age, diabetes, tobacco use, arterial hypertension, hypercholesterolemia, hypertriglyceridemia, decreased high-density lipoprotein, some hypercoaguable states, sedentary life-style, and elevated plasma homocysteine. The study of lipid metabolism has dominated research into atherosclerosis etiology for decades, although now it is widely recognized that a large number of people with symptomatic atherosclerotic disease have no detectable evidence of abnormal lipid metabolism [1, 2]. Elevation in plasma homocysteine has also been widely studied as an independent risk factor for atherosclerosis. A description of the metabolism of homocysteine, its relationship to vascular disease, evidence supporting its role as an independent risk factor for atherosclerotic vascular disease, and the potential role of treatment will form the basis for this review.
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OMAR, EFFAT, NURUL AISHAH MUHAMMAD, NURUL AIN ABU BAKAR, and HAPIZAH NAWAWI. "PREVENTIVE EFFECTS OF TOCOTRIENOL-ENRICHED MIXED FRACTION ON PLAQUE FORMATION AND STABILITY IN EARLY AND ESTABLISHED ATHEROSCLEROSIS." Malaysian Applied Biology 51, no. 1 (March 31, 2022): 21–28. http://dx.doi.org/10.55230/mabjournal.v51i1.1995.
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Atherosclerosis is the underlying pathology for cardiovascular disease. The preventive effects of tocotrienol-enriched mixed fraction (TEMF) on atherogenesis remains unclear. Objective: To investigate the preventive effects of TEMF supplementation on early and established atherosclerosis. Methods: Twenty New Zealand white rabbits were divided into TEMF (n=10) and placebo (n=10) groups. Treatments were given by oral gavage for 8 weeks followed by 1% high cholesterol diet (HCD) for another two (to induce early atherosclerosis) or eight weeks (established atherosclerosis). At the end of the study, the aorta was dissected, stained with Sudan IV, and qualitatively analysed for the atherosclerotic lesion. Immunohistochemistry was performed to detect expression of interleukin-6 (IL-6), CRP, nuclear factor kappa beta, E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion protein-1 (VCAM-1), smooth muscle actin (SMA) and matrix metalloproteinase-12 (MMP-12). Results: In both early and established atherosclerosis groups, there was a significant reduction of atherosclerotic lesions in TEMF compared to placebo. Atherogenic biomarkers; IL-6, CRP, E-selectin, SMA, and MMP-12 were reduced with TEMF supplementation in established atherosclerosis (p<0.05). Neutral effects were seen in early atherosclerosis group. TEMF supplementation in the preventive setting decreased atherosclerosis formation and reduces endothelial inflammation in established atherosclerosis lesions, while increasing plaque stability.
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Zhu, Yuhua, Xuemei Xian, Zhenzhen Wang, Yingchao Bi, Quangang Chen, Xufeng Han, Daoquan Tang, and Renjin Chen. "Research Progress on the Relationship between Atherosclerosis and Inflammation." Biomolecules 8, no. 3 (August 23, 2018): 80. http://dx.doi.org/10.3390/biom8030080.
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Atherosclerosis is a chronic inflammatory disease; unstable atherosclerotic plaque rupture, vascular stenosis, or occlusion caused by platelet aggregation and thrombosis lead to acute cardiovascular disease. Atherosclerosis-related inflammation is mediated by proinflammatory cytokines, inflammatory signaling pathways, bioactive lipids, and adhesion molecules. This review discusses the effects of inflammation and the systemic inflammatory signaling pathway on atherosclerosis, the role of related signaling pathways in inflammation, the formation of atherosclerosis plaques, and the prospects of treating atherosclerosis by inhibiting inflammation.
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Kim, Jong S., Yeon-Jung Kim, Sung-Ho Ahn, and Bum J. Kim. "Location of cerebral atherosclerosis: Why is there a difference between East and West?" International Journal of Stroke 13, no. 1 (May 4, 2016): 35–46. http://dx.doi.org/10.1177/1747493016647736.
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Intracranial atherosclerosis is more prevalent in Asian patients, whereas extracranial atherosclerosis is more common in individuals from western countries. The reasons for this discrepancy remain unknown. We reviewed the relevant literature and discussed the currently available information. Although the study population, diagnostic modality, and risk factor definitions differ between studies, hypercholesterolemia is more correlated with extracranial atherosclerosis than intracranial atherosclerosis. The difference in hypercholesterolemia prevalence is one of the main reasons for racial differences. Intracranial arteries contain higher antioxidant level than extracranial arteries and may be more vulnerable to risk factors for antioxidant depletion (e.g., metabolic syndrome and diabetes mellitus). Intracranial arteries may be vulnerable to factors associated with hemodynamic stress (e.g., advanced, salt-retaining hypertension and arterial tortuosity) because of a smaller diameter, thinner media and adventitia, and fewer elastic medial fibers than extracranial arteries. Additionally, non-atherosclerotic arterial diseases (e.g., moyamoya disease) that commonly occur in the intracranial arteries of East Asians may contaminate the reports of intracranial atherosclerosis cases. Genes, including RNF 213 or those associated with high salt sensitivity, may also explain racial differences in atherosclerotic location. To understand racial differences, further well-designed studies on various risk and genetic factors should be performed in patients with cerebral atherosclerosis. Additionally, improvements in diagnostic accuracy via advancements in imaging technologies and increased genetic data will aid in the differentiation of atherosclerosis from non-atherosclerotic intracranial diseases.
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Zhao, Bing, and Lihong Gong. "Exploring the Treatment of Coronary Artery Atherosclerosis from the Direction of Inflammatory Vesicles with Wind-Extinguishing and Phlegm-Resolving Medicine." Journal of Clinical and Nursing Research 6, no. 1 (January 19, 2022): 105–10. http://dx.doi.org/10.26689/jcnr.v6i1.2934.
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Atherosclerosis is a fundamental pathological change in coronary heart disease, with vulnerable plaque formation leading to decreased plaque stability and plaque rupture, and is a major cause of acute cardiovascular events. The inflammatory response is an important mechanism in the development and progression of atherosclerosis, and plaque stability is closely related to the inflammatory response. In recent years, the role of NLRP3 inflammatory vesicles, which are involved in macrophage foaminess, in the inflammatory response to atherosclerosis has received increasing attention. Chinese medicine is able to modulate inflammatory vesicles to improve atherosclerotic plaque stability, showing good promise in the prevention and treatment of atherosclerotic vulnerable plaques. Based on the role of inflammatory vesicles in atherosclerosis and the results of previous studies that wind-extinguishing and phlegm-resolving medicine can effectively modulate the inflammatory response to intervene in the treatment of atherosclerosis, this paper aims to investigate the treatment of coronary atherosclerosis by wind-extinguishing and phlegm-resolving medicine from the direction of inflammatory vesicles.
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Patel, Divyakshi, Gauri Mahajan, and Neeraj Mahajan. "The link between gut microbiota and atherosclerosis." Indian Journal of Clinical Anatomy and Physiology 10, no. 3 (October 15, 2023): 145–48. http://dx.doi.org/10.18231/j.ijcap.2023.032.
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Infections have been linked to development of cardiovascular complaint and atherosclerosis. Cardio vascular conditions like atherosclerosis are the major cause of mortality and morbidity in the ultramodern society. The rupture of atherosclerotic plaque can induce thrombus conformation, which is the main cause of acute cardiovascular events. Lately, numerous studies have demonstrated that there are some connections between microbiota and atherosclerosis. There are three metabolite pathways by which gut microbiota can affect atherosclerosis. Either original or distant- causing inflammation which might lead to atherosclerotic plaque formation and rupture. Second, metabolism of lipids and cholesterol by gut microbiota can affect atheromatous atheromatous plaque conformation. Third, diet and specific factors that are metabolized by gut microbiota can have various effects on atherosclerosis; for illustration, salutary fiber is beneficial, whereas the bacterial metabolite trimethylamine- N- oxide (TMAO) is considered dangerous. We'll conclude by discussing new remedial strategies for targeting gut microbiota to ameliorate atherosclerosis and related cardiovascular issues.
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SHAN, Zhen, Chen YAO, Zi-lun LI, Yuan TENG, Wen LI, Jin-song WANG, Cai-sheng YE, et al. "Differentially expressed microRNAs at different stages of atherosclerosis in ApoE-deficient mice." Chinese Medical Journal 126, no. 3 (February 2013): 515–20. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20122289.
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Background Atherosclerosis is the primary cause of cardiovascular disease, carotid artery disease, and peripheral vascular disease. However, it is hard to obtain human arterial tissue at different stages of atherosclerosis for a systematic study. The ApoE-deficient (ApoE-/-) mice predictably develop spontaneous atherosclerotic plaques with numerous features similar to the human lesions and contain nearly the entire spectrum of lesions observed during atherogenesis in humans. MicroRNA expression profiles at different stages of atherosclerosis in ApoE-deficient mice were screened to find out the differentially expressed microRNAs. Methods ApoE-deficient mice were euthanized at 4, 8, and 20 weeks of age and divided into three groups according to the three time points, including groups A4 (fed a Western-type diet for 0 week), A8 (fed a Western-type diet for 4 weeks), and A20 (fed a Western-type diet for 16 weeks). Atherosclerotic lesions were analyzed. Fifteen aortas were collected and combined into three pools (five aortas in one pool) in each group. MicroRNA microarray analysis was replicated thrice in each group. The threshold of fold change ≥2.0 was used to screen up or down-regulated microRNAs. Differentially expressed microRNAs were subsequently verified with quantitative real-time polymerase chain reaction. Those increasingly up or down-regulated microRNAs during the progression of atherosclerosis were selected. Results Atherosclerotic lesions first appeared in the aortic arch in group A8. Severe atherosclerotic lesions were observed in group A20. In group A8, seven MicroRNAs were up-regulated while two were down-regulated. In group A20, 15 microRNAs were up-regulated while two were down-regulated. miR-34a-5p and miR-497-5p were increasingly up-regulated, while miR-434-3p was progressively down-regulated when atherosclerosis progressed. Conclusions In this study, we described that microRNAs are differentially expressed at different stages of atherosclerosis in ApoE-deficient mice. Those increasingly up or down-regulated microRNAs during the progression of atherosclerosis may play an important role in the pathogenesis of atherosclerosis and provide us opportunities for investigating atherosclerosis from early to advanced stages.
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Song, Boce, Yulong Bie, Haoxin Feng, Beili Xie, Mingwang Liu, and Fuhai Zhao. "Inflammatory factors driving atherosclerotic plaque progression new insights." Journal of Translational Internal Medicine 10, no. 1 (March 1, 2022): 36–47. http://dx.doi.org/10.2478/jtim-2022-0012.
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Abstract Coronary atherosclerosis is a chronic inflammatory disease that can lead to varying degrees of blood flow obstruction and a common pathophysiological basis of cardiovascular disease. Inflammatory factors run through the whole process of atherosclerotic lesions. Macrophages, T cells, and neutrophils play important roles in the process of atherosclerotic inflammation. Considering the evolutionary characteristics, atherosclerosis can be divided into different stages as early atherosclerotic plaque, plaque formation stage, and plaque rupture stage. In this paper, the changes in inflammatory cells at different stages of lesions and their related mechanisms are discussed, which can provide new insights from a clinical to bench perspective for atherosclerosis me chanism.
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Wei, Chen, Yubing Shi, Hongge Zhang, Huihui Fang, Yangjie Zuo, and Jing Dong. "The role of endothelial cells in the formation and progression of atherosclerosis." International Journal of Multidisciplinary Research and Growth Evaluation 4, no. 5 (2023): 732–37. http://dx.doi.org/10.54660/.ijmrge.2023.4.5.732-737.
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The functions of endothelial cells include physical barriers, sensory organs and endocrine organs, and all three of its functional abnormalities will lead to endothelial cell dysfunction, which will lead to the formation of atherosclerotic lesion initiation and continue to play an important role in the atherosclerotic process. Based on domestic and international research on endothelial cells and atherosclerosis, various causes of endothelial cell dysfunction and their important roles in the process of atherosclerosis will be explored, analyzed and synthesized, and finally the relationship between endothelial cell damage and the formation of atherosclerosis will be comprehensively analyzed at the molecular and individual levels, in order to provide new ideas and methods for the prevention and treatment of atherosclerosis.
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Szabo, Helga, Marton Piroska, Anita Hernyes, Luca Zoldi, Janos Juhasz, Balazs Ligeti, Nora Makra, et al. "The Relationship between Atherosclerosis and Gut Microbiome in Patients with Obstructive Sleep Apnoea." Applied Sciences 12, no. 22 (November 11, 2022): 11484. http://dx.doi.org/10.3390/app122211484.
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Background: Obstructive sleep apnoea (OSA) and gut dysbiosis are known risk factors for atherosclerosis. However, only very few studies have been focused on the relationship between OSA, atherosclerosis, and the intestinal microbiome, all in animal models. Methods: Twenty-two patients with OSA, 16 with and 6 without carotid atherosclerosis were involved in the study. After a diagnostic sleep examination, the intima media thickness (IMT) was measured and plaques were found using carotid ultrasound. Blood was also drawn for metabolic profile, and a stool sample was provided for 16S ribosomal RNA microbiome investigation. Results: An increased maximal common carotid artery (CCA) IMT was significantly associated with decreased phylum-level diversity. The level of Peptostreptococcaceae was significantly lower in atherosclerotic subjects. Some other candidate microbes appeared in the two groups at the genus level as well: Bilophila, Romboutsia, Slackia, and Veillonella in the non-atherosclerotic group; and Escherichia-Shigella, Prevotella, and Ruminococcaceae in the atherosclerotic group. Conclusions: This is the first pilot research to analyze the association between the gut microbiome and atherosclerosis in adult patients with OSA with and without carotid atherosclerosis. Dysbiosis and individual bacteria may contribute to the development of carotid atherosclerosis in patients with OSA. Further investigations are necessary to reveal a more precise background in a larger sample.
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Tsui, Pi-Fen, Chin-Sheng Lin, Ling-Jun Ho, and Jenn-Haung Lai. "Spices and Atherosclerosis." Nutrients 10, no. 11 (November 10, 2018): 1724. http://dx.doi.org/10.3390/nu10111724.
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Cardiovascular disease is one of the leading causes of death and disability in the world. Atherosclerosis, characterized by lipid accumulation and chronic inflammation in the vessel wall, is the main feature of cardiovascular disease. Although the amounts of fruits and vegetables present in the diets vary by country, diets, worldwide, contain large amounts of spices; this may have positive or negative effects on the initiation and development of atherosclerosis. In this review, we focused on the potential protective effects of specific nutrients from spices, such as pepper, ginger, garlic, onion, cinnamon and chili, in atherosclerosis and atherosclerotic cardiovascular disease. The mechanisms, epidemiological analysis, and clinical studies focusing on a variety of spices are covered in this review. Based on the integrated information, we aimed to raise specific recommendations for people with different dietary styles for the prevention of atherosclerotic cardiovascular disease through dietary habit adjustments.
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Eitzman, Daniel T., Randal J. Westrick, Zuojun Xu, Julia Tyson, and David Ginsburg. "Plasminogen activator inhibitor-1 deficiency protects against atherosclerosis progression in the mouse carotid artery." Blood 96, no. 13 (December 15, 2000): 4212–15. http://dx.doi.org/10.1182/blood.v96.13.4212.
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Abstract Dissolution of the fibrin blood clot is regulated in large part by plasminogen activator inhibitor-1 (PAI-1). Elevated levels of plasma PAI-1 may be an important risk factor for atherosclerotic vascular disease and are associated with premature myocardial infarction. The role of the endogenous plasminogen activation system in limiting thrombus formation following atherosclerotic plaque disruption is unknown. This study found that genetic deficiency for PAI-1, the primary physiologic regulator of tissue-type plasminogen activator (tPA), prolonged the time to occlusive thrombosis following photochemical injury to carotid atherosclerotic plaque in apolipoprotein E-deficient (apoE−/−) mice. However, anatomic analysis revealed a striking difference in the extent of atherosclerosis at the carotid artery bifurcation between apoE−/− mice and mice doubly deficient for apoE and PAI-1 (PAI-1−/−/apoE−/−). Consistent with a previous report, PAI-1+/+/apoE−/−and PAI-1−/−/apoE−/− mice developed similar atherosclerosis in the aortic arch. The marked protection from atherosclerosis progression at the carotid bifurcation conferred by PAI-1 deficiency suggests a critical role for PAI-1 in the pathogenesis of atherosclerosis at sites of turbulent flow, potentially through the inhibition of fibrin clearance. Consistent with this hypothesis, intense fibrinogen/fibrin staining was observed in atherosclerotic lesions at the carotid bifurcation compared to the aortic arch. These observations identify significant differences in the pathogenesis of atherosclerosis at varying sites in the vascular tree and suggest a previously unappreciated role for the plasminogen activation system in atherosclerosis progression at sites of turbulent flow.
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Eitzman, Daniel T., Randal J. Westrick, Zuojun Xu, Julia Tyson, and David Ginsburg. "Plasminogen activator inhibitor-1 deficiency protects against atherosclerosis progression in the mouse carotid artery." Blood 96, no. 13 (December 15, 2000): 4212–15. http://dx.doi.org/10.1182/blood.v96.13.4212.h8004212_4212_4215.
Full textAbstract:
Dissolution of the fibrin blood clot is regulated in large part by plasminogen activator inhibitor-1 (PAI-1). Elevated levels of plasma PAI-1 may be an important risk factor for atherosclerotic vascular disease and are associated with premature myocardial infarction. The role of the endogenous plasminogen activation system in limiting thrombus formation following atherosclerotic plaque disruption is unknown. This study found that genetic deficiency for PAI-1, the primary physiologic regulator of tissue-type plasminogen activator (tPA), prolonged the time to occlusive thrombosis following photochemical injury to carotid atherosclerotic plaque in apolipoprotein E-deficient (apoE−/−) mice. However, anatomic analysis revealed a striking difference in the extent of atherosclerosis at the carotid artery bifurcation between apoE−/− mice and mice doubly deficient for apoE and PAI-1 (PAI-1−/−/apoE−/−). Consistent with a previous report, PAI-1+/+/apoE−/−and PAI-1−/−/apoE−/− mice developed similar atherosclerosis in the aortic arch. The marked protection from atherosclerosis progression at the carotid bifurcation conferred by PAI-1 deficiency suggests a critical role for PAI-1 in the pathogenesis of atherosclerosis at sites of turbulent flow, potentially through the inhibition of fibrin clearance. Consistent with this hypothesis, intense fibrinogen/fibrin staining was observed in atherosclerotic lesions at the carotid bifurcation compared to the aortic arch. These observations identify significant differences in the pathogenesis of atherosclerosis at varying sites in the vascular tree and suggest a previously unappreciated role for the plasminogen activation system in atherosclerosis progression at sites of turbulent flow.
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Qiao, Z., J. Ren, and H. Chen. "Simvastatin Reduces Expression and Activity of Lipoprotein-Associated Phospholipase A2 in the Aorta of Hypercholesterolaemic Atherosclerotic Rabbits." Journal of International Medical Research 37, no. 4 (August 2009): 1029–37. http://dx.doi.org/10.1177/147323000903700407.
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Lipoprotein-associated phospholipase A2 (Lp-PLA2) contributes to atherosclerotic plaque instability and subsequent sudden coronary death. Statins are associated with decreased stroke risk and may improve stability of atherosclerotic plaques. The present study investigated the effect of simvastatin on expression of Lp-PLA2 levels in atherosclerotic plaques and on Lp-PLA2 activity in atherosclerotic aortas. Rabbits were a fed chow (control group) or a high-cholesterol diet (atherosclerosis group) for 12 weeks. An additional group on the high-cholesterol diet received simvastatin (5 mg/kg per day) for the last 4 weeks (simvastatin group). Lp-PLA2 activity in plasma and atherosclerotic aortas was significantly higher in the atherosclerosis group than in the control group and, consistent with this, abundant Lp-PLA2 protein was detected in plaques in the atherosclerosis group. Simvastatin significantly reduced Lp-PLA2 activity in plasma and aorta tissue, and reduced Lp-PLA2 protein level in atherosclerotic plaques. Whereas there was no significant difference in total atherosclerotic lesion area between simvastatin and atherosclerosis groups, simvastatin significantly reduced macrophage content, lipid retention and the intima/media ratio but increased the content of smooth muscle cells in atherosclerotic lesions. Thus, statin treatment markedly reduced Lp-PLA2 in both plasma and atherosclerotic plaques. This was associated with attenuation of the local inflammatory response and improved plaque stability.
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Kishimoto, Yoshimi, Kazuo Kondo, and Yukihiko Momiyama. "The Protective Role of Sestrin2 in Atherosclerotic and Cardiac Diseases." International Journal of Molecular Sciences 22, no. 3 (January 26, 2021): 1200. http://dx.doi.org/10.3390/ijms22031200.
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Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that is induced by various stresses such as hypoxia, DNA damage, and oxidative stress. Sestrin2 is also suggested to be associated with aging. Sestrin2 is expressed and secreted mainly by macrophages, endothelial cells, and cardiomyocytes. Sestrin2 plays an important role in suppressing the production and accumulation of ROS, thus protecting cells from oxidative damage. Since sestrin2 is reported to have anti-oxidant and anti-inflammatory properties, it may play a protective role against the progression of atherosclerosis and may be a potential therapeutic target for the amelioration of atherosclerosis. Regarding the association between blood sestrin2 levels and atherosclerotic disease, the blood sestrin2 levels in patients with CAD or carotid atherosclerosis were reported to be high. High blood sestrin2 levels in patients with such atherosclerotic disease may reflect a compensatory response to increased oxidative stress and may help protect against the progression of atherosclerosis. This review describes the protective role of sestrin2 against the progression of atherosclerotic and cardiac diseases.
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Burger, Fabienne, Daniela Baptista, Aline Roth, Karim J. Brandt, and Kapka Miteva. "The E3 Ubiquitin Ligase Peli1 Deficiency Promotes Atherosclerosis Progression." Cells 11, no. 13 (June 23, 2022): 2014. http://dx.doi.org/10.3390/cells11132014.
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Background: Atherosclerosis is a chronic inflammatory vascular disease and the main cause of death and morbidity. Emerging evidence suggests that ubiquitination plays an important role in the pathogenesis of atherosclerosis including control of vascular inflammation, vascular smooth muscle cell (VSMC) function and atherosclerotic plaque stability. Peli1 a type of E3 ubiquitin ligase has emerged as a critical regulator of innate and adaptive immunity, however, its role in atherosclerosis remains to be elucidated. Methods: Apoe−/− mice and Peli1-deficient Apoe−/− Peli1−/− mice were subject to high cholesterol diet. Post sacrifice, serum was collected, and atherosclerotic plaque size and parameters of atherosclerotic plaque stability were evaluated. Immunoprofiling and foam cell quantification were performed. Results: Peli1 deficiency does not affect atherosclerosis lesion burden and cholesterol levels, but promotes VSMCs foam cells formation, necrotic core expansion, collagen, and fibrous cap reduction. Apoe−/− Peli1–/– mice exhibit a storm of inflammatory cytokines, expansion of Th1, Th1, Th17, and Tfh cells, a decrease in regulatory T and B cells and induction of pro-atherogenic serum level of IgG2a and IgE. Conclusions: In the present study, we uncover a crucial role for Peli1 in atherosclerosis as an important regulator of inflammation and VSMCs phenotypic modulation and subsequently atherosclerotic plaque destabilization.
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Gencer, Selin, Bryce R. Evans, Emiel P. C. van der Vorst, Yvonne Döring, and Christian Weber. "Inflammatory Chemokines in Atherosclerosis." Cells 10, no. 2 (January 25, 2021): 226. http://dx.doi.org/10.3390/cells10020226.
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Atherosclerosis is a long-term, chronic inflammatory disease of the vessel wall leading to the formation of occlusive or rupture-prone lesions in large arteries. Complications of atherosclerosis can become severe and lead to cardiovascular diseases (CVD) with lethal consequences. During the last three decades, chemokines and their receptors earned great attention in the research of atherosclerosis as they play a key role in development and progression of atherosclerotic lesions. They orchestrate activation, recruitment, and infiltration of immune cells and subsequent phenotypic changes, e.g., increased uptake of oxidized low-density lipoprotein (oxLDL) by macrophages, promoting the development of foam cells, a key feature developing plaques. In addition, chemokines and their receptors maintain homing of adaptive immune cells but also drive pro-atherosclerotic leukocyte responses. Recently, specific targeting, e.g., by applying cell specific knock out models have shed new light on their functions in chronic vascular inflammation. This article reviews recent findings on the role of immunomodulatory chemokines in the development of atherosclerosis and their potential for targeting.
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Kovacic, Sanja, and Mirjana Bakran. "Genetic Susceptibility to Atherosclerosis." Stroke Research and Treatment 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/362941.
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Atherosclerosis is a complex multifocal arterial disease involving interactions of multiple genetic and environmental factors. Advances in techniques of molecular genetics have revealed that genetic ground significantly influences susceptibility to atherosclerotic vascular diseases. Besides further investigations of monogenetic diseases, candidate genes, genetic polymorphisms, and susceptibility loci associated with atherosclerotic diseases have been identified in recent years, and their number is rapidly increasing. This paper discusses main genetic investigations fields associated with human atherosclerotic vascular diseases. The paper concludes with a discussion of the directions and implications of future genetic research in arteriosclerosis with an emphasis on prospective prediction from an early age of individuals who are predisposed to develop premature atherosclerosis as well as to facilitate the discovery of novel drug targets.
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Saranchina, J. V., S. V. Dutova, O. Y. Kilina, N. V. Khanarin, and T. S. Kulakova. "Features of interleukin-19 production in patients with atherosclerosis." Siberian Journal of Clinical and Experimental Medicine 36, no. 2 (July 7, 2021): 52–60. http://dx.doi.org/10.29001/2073-8552-2021-36-2-52-60.
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Objective. To study the features of local and systemic production of interleukin-19 in patients with atherosclerosis.Material and Methods. The study comprised a total of 46 patients (26 women and 20 men) treated for arterial hypertension in the therapeutic department of Republican Clinical Hospital named after G.Y. Remishevskaya. The mean age of subjects was 63.4 ± 3.2 years. The control group included 40 patients (23 women and 17 men aged 44.7 ± 5.5 years) who did not have atherosclerosis. Samples of atherosclerotic plaques and venous blood were examined. Atherosclerotic plaques were obtained by endarterectomy and then subjected to homogenization followed by enzymatic hydrolysis for 1 h at 37 °C with collagenase IV in the presence of proteinase III inhibitors. The serum levels of cytokines (in the control group and in patients with atherosclerosis) and in the atherosclerotic plaque homogenate (in patients with atherosclerosis) were determined by ELISA. To assess the cytokine-producing capacity of blood leukocytes and white blood cells isolated from atherosclerotic plaques, spontaneous and phytohemagglutinin (PHA)-induced cytokine production was determined when the cells were cultured in RPMI-1640.Results. The serum levels of IL-19 did not significantly differ between the patients with atherosclerosis and the control group. A statistically significant two-fold increase in the spontaneous expression of IL-19 by blood leukocytes was observed in the group of patients with atherosclerosis in comparison with the control group. When comparing the contents of IL-19 in blood serum and atherosclerotic plaque homogenate in patients with atherosclerosis, no statistically significant differences were found (p = 0.182). The level of PHA-induced IL-19 production by the atherosclerotic plaque white blood cells was significantly lower than that of blood leucocytes.Conclusion. The study showed that the reserve capacity for IL-19 synthesis in the atherosclerotic plaque white blood cells decreases leading to the progression of inflammation. The obtained results suggest that IL-19 plays the anti-atherogenic role and its production is involved in the maintaining the mechanisms for down-regulation of inflammation in atherosclerotic plaques.
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Henriques, Joana, Ana M. Amaro, and Ana P. Piedade. "Understanding Atherosclerosis Pathophysiology: Can Additive Manufacturing Be Helpful?" Polymers 15, no. 3 (January 17, 2023): 480. http://dx.doi.org/10.3390/polym15030480.
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Atherosclerosis is one of the leading causes of death worldwide. Although this subject arouses much interest, there are limitations associated with the biomechanical investigation done in atherosclerotic tissues, namely the unstandardized tests for the mechanical characterization of these tissues and the inherent non-consensual results obtained. The variability of tests and typologies of samples hampers direct comparisons between results and hinders the complete understanding of the pathologic process involved in atherosclerosis development and progression. Therefore, a consensual and definitive evaluation of the mechanical properties of healthy and atherosclerotic blood vessels would allow the production of physical biomodels that could be used for surgeons’ training and personalized surgical planning. Additive manufacturing (AM), commonly known as 3D printing, has attracted significant attention due to the potential to fabricate biomodels rapidly. However, the existing literature regarding 3D-printed atherosclerotic vascular models is still very limited. Consequently, this review intends to present the atherosclerosis disease and the consequences of this pathology, discuss the mechanical characterization of atherosclerotic vessels/plaques, and introduce AM as a potential strategy to increase the understanding of atherosclerosis treatment and pathophysiology.
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Millon, Antoine, Emmanuelle Canet-Soulas, Loic Boussel, Zahi Fayad, and Philippe Douek. "Animal models of atherosclerosis and magnetic resonance imaging for monitoring plaque progression." Vascular 22, no. 3 (June 2014): 221–37. http://dx.doi.org/10.1177/1708538113478758.
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Atherosclerosis, the main cause of heart attack and stroke, is the leading cause of death in most modern countries. Preventing clinical events depends on a better understanding of the mechanism of atherosclerotic plaque destabilization. Our knowledge on the characteristics of vulnerable plaques in humans has grown past decades. Histological studies have provided a precise definition of high-risk lesions and novel imaging methods for human atherosclerotic plaque characterization have made significant progress. However the pathological mechanisms leading from stable lesions to the formation of vulnerable plaques remain uncertain and the related clinical events are unpredictable. An animal model mimicking human plaque destablization is required as well as an in vivo imaging method to assess and monitor atherosclerosis progression. Magnetic resonance imaging (MRI) is increasingly used for in vivo assessment of atherosclerotic plaques in the human carotids. MRI provides well-characterized morphological and functional features of human atherosclerotic plaque which can be also assessed in animal models. This review summarizes the most common species used as animal models for experimental atherosclerosis, the techniques to induce atherosclerosis and to obtain vulnerable plaques, together with the role of MRI for monitoring atherosclerotic plaques in animals.
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Tu, Shuangshuang, Wenming He, Jinru Han, Aiguo Wu, and Wenzhi Ren. "Advances in imaging and treatment of atherosclerosis based on organic nanoparticles." APL Bioengineering 6, no. 4 (December 1, 2022): 041501. http://dx.doi.org/10.1063/5.0127835.
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Atherosclerosis, a systemic chronic inflammatory disease, can lead to thrombosis and vascular occlusion, thereby inducing a series of serious vascular diseases. Currently, distinguishing unstable plaques early and achieving more effective treatment are the two main clinical concerns in atherosclerosis. Organic nanoparticles have great potential in atherosclerotic imaging and treatment, showing superior biocompatibility, drug-loading capacity, and synthesis. This article illustrates the process of atherosclerosis onset and the key targeted cells, then systematically summarizes recent progress made in organic nanoparticle-based imaging of different types of targeted cells and therapeutic methods for atherosclerosis, including optical and acoustic-induced therapy, drug delivery, gene therapy, and immunotherapy. Finally, we discuss the major impediments that need to be addressed in future clinical practice. We believe this article will help readers to develop a comprehensive and in-depth understanding of organic nanoparticle-based atherosclerotic imaging and treatment, thus advancing further development of anti-atherosclerosis therapies.
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Zhang, Lili, Lihua Li, Yalan Li, Han Jiang, Zhen Sun, Guangyao Zang, Yongjiang Qian, Chen Shao, and Zhongqun Wang. "Disruption of COMMD1 accelerates diabetic atherosclerosis by promoting glycolysis." Diabetes and Vascular Disease Research 20, no. 1 (January 2023): 147916412311590. http://dx.doi.org/10.1177/14791641231159009.
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Aims Diabetes will lead to serious complications, of which atherosclerosis is the most dangerous. This study aimed to explore the mechanisms of diabetic atherosclerosis. Methods ApoE−/− mice were fed with an high-fat diet diet and injected with streptozotocin to establish an in vivo diabetic atherosclerotic model. RAW 264.7 cells were treated with oxidized low-density lipoprotein particles (ox-LDL) and high glucose to produce an in vitro diabetic atherosclerotic model. Results In this study, we showed that diabetes promoted the progression of atherosclerosis in ApoE−/− mice and that high glucose potentiates macrophage proinflammatory activation and foam cell formation. Mechanistically, Copper metabolism MURR1 domain-containing 1(COMMD1) deficiency increased proinflammatory activation and foam cell formation, characterized by increased glycolysis, and then accelerated the process of atherosclerosis. Furthermore, 2-Deoxy-D-glucose (2-DG) reversed this effect. Conclusion Taken together, we provided evidence that the lack of COMMD1 accelerates diabetic atherosclerosis via mediating the metabolic reprogramming of macrophages. Our study provides evidence of a protective role for COMMD1 and establishes COMMD1 as a potential therapeutic strategy in patients with diabetic atherosclerosis.
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Mohmand-Borkowski, Adam, and Tomasz Rozmyslowicz. "Immunohistochemical Localization of Fibroblast Activation Protein in Coronary Arteries with Different Forms of Atherosclerosis." Metabolites 14, no. 11 (October 25, 2024): 573. http://dx.doi.org/10.3390/metabo14110573.
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Background: Fibroblast activation protein (FAP) is a cell surface glycoprotein expressed by myofibroblasts in areas of active tissue remodeling. It plays a potentially important role in cardiac remodeling, atherosclerotic plaque formation, and plaque rupture. Given the distinct pathophysiology and morphology of different forms of atherosclerosis, we analyzed FAP expression in human coronary vessels with no coronary artery disease, atherosclerotic plaques at different levels of progression, and other distinct forms of coronary disease in post bypass vein grafting and cardiac allograft vasculopathy after a heart transplant. Methods: Immunohistochemical staining with monoclonal F19 mouse anti-human FAP antibody was performed to identify FAP in human atherosclerotic plaques, coronary bypass atherosclerosis, and post-transplant arteriosclerosis. The presence and distribution of FAP in different types and stages of human atherosclerosis were compared. Results: There was no FAP staining in patients with no significant coronary disease. All different types of human atherosclerotic lesioning lesions showed the presence of FAP expression, with different staining patterns in advanced atherosclerotic plaque, vein graft atherosclerosis lesions, and arteriosclerosis after a heart transplant. Conclusions: These data suggest that FAP may be a potential diagnostic marker and target for interventions, not only in coronary atherosclerotic plaque, but also in other forms of coronary disease, which have distinct pathophysiologies and currently limited treatment options.
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Lu, Shynie. "Interferon regulatory factor 3 is a potential biomarker to predict the process of atherosclerosis." BIO Web of Conferences 61 (2023): 01025. http://dx.doi.org/10.1051/bioconf/20236101025.
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Cardiovascular diseases is one of the major public health and medical concerns globally. Atherosclerosis is a condition where plaque build-up narrows the blood vessels, ultimately preventing sufficient blood flow to the heart. In current research, the role played by the human innate immune system in the development of atherosclerosis is a topic of interest. Although the specific relations require further studies, macrophages have been identified to play a key role in the progression of atherosclerosis due to their ability to mediate inflammation. Nevertheless, the mechanism that how macrophages cause inflammatory responses in atherosclerotic process and what is the risk factor that can describe the inflammation in clinic still remains unclear. This paper reviews the mechanism of macrophages to trigger inflammation and their relationships to atherosclerosis. In this study, Interferon Regulatory Factor 3 (IRF3) and its-related cytokine interleukin 1β was found to be upregulated in patients with acute coronary disease. Afterwards, the over-expressed IRF3 level and its RNA transcription was further confirmed in atherosclerotic ApoE-/-mice. Our results indicated that IRF3 was up-regulated during atherosclerotic process, which might be a potential biomarker of atherosclerosis and its-related coronary disease in clinic.
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Bozidar, Kocmur. "Atherosclerosis and wine." Journal of Cardiovascular Medicine and Cardiology 11, no. 1 (March 12, 2024): 018–21. http://dx.doi.org/10.17352/2455-2976.000204.
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One of the most important risk factors for the origin and development of atherosclerosis is certainly excessive intake of fat in everyday nutrition. This risk factor, and the way it affects the origin and development of atherosclerosis, is described in the article “Atherosclerosis and lymph/risk factors”. In this article, based on verified and proven facts, it is suggested that the primary causes and initiators of atherosclerotic changes in the arterial system of the circulatory system are chylomicrons, especially large ones, which occur under the influence of several risk factors.
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Meiliana, Anna, and Andi Wijaya. "Inflammation and Atherosclerosis: Current Pathogenesis." Indonesian Biomedical Journal 4, no. 2 (August 1, 2012): 73. http://dx.doi.org/10.18585/inabj.v4i2.165.
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BACKGROUND: The inflammatory nature of atherosclerosis is well established but the agent(s) that incite inflammation in the artery wall remain largely unknown.CONTENT: Chronic inflammation is recognized as a major driving force in atherogenesis. The sites of atherosclerotic plaque development in the arterial wall are characterized by cholesterol accumulation and infiltration of peripheral blood monocytes, which gradually differentiate into macrophages. Cholesterol crystals, the common constituents of atherosclerotic lesions, include NLRP3 inflammasome activation and IL-1β secretion in human macrophages, promote an inflammatory milieu and thus drive lesion progression. Consequently, the cholesterol crystal-induced inflammasome activation may represent an important link between cholesterol metabolism and inflammation in atherosclerotic lesions. SUMMARY: The crystalline cholesterol acts as an endogenous danger signal and its deposition in arteries or elsewhere is an early cause rather than a late consequence of inflammation. The cholesterol crystal-induced inflammasome activation in macrophages may represent an important link between cholesterol metabolism and inflammation in atherosclerotic lesions. This finding provides new insights into the pathogenesis of atherosclerosis and indicates new potential molecular targets for the therapy of this disease.KEYWORDS: atherosclerosis, inflammation, neutrophil, macrophages, inflammasome, cholesterol crystal
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Marchini, Timoteo, Tijani Abogunloko, and Dennis Wolf. "Modulating Autoimmunity against LDL: Development of a Vaccine against Atherosclerosis." Hämostaseologie 41, no. 06 (December 2021): 447–57. http://dx.doi.org/10.1055/a-1661-1908.
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AbstractAtherosclerosis is a chronic inflammatory disease of the arterial wall that leads to the build-up of occluding atherosclerotic plaques. Its clinical sequelae, myocardial infarction and stroke, represent the most frequent causes of death worldwide. Atherosclerosis is a multifactorial pathology that involves traditional risk factors and chronic low-grade inflammation in the atherosclerotic plaque and systemically. This process is accompanied by a strong autoimmune response that involves autoreactive T cells in lymph nodes and atherosclerotic plaques, as well as autoantibodies that recognize low-density lipoprotein (LDL) and its main protein component apolipoprotein B (ApoB). In the past 60 years, numerous preclinical observations have suggested that immunomodulatory vaccination with LDL, ApoB, or its peptides has the potential to specifically dampen autoimmunity, enhance tolerance to atherosclerosis-specific antigens, and protect from experimental atherosclerosis in mouse models. Here, we summarize and discuss mechanisms, challenges, and therapeutic opportunities of immunomodulatory vaccination and other strategies to enhance protective immunity in atherosclerosis.
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Yan, Sishan, Teng Wu, Ning Li, Lingyi Zhang, Jun Song, Yunzheng Xu, Shumei Wang, et al. "Protective Effects of Chinese Traditional Medicine Longhu Rendan against Atherosclerosis via Negative Regulation of LOX-1." Evidence-Based Complementary and Alternative Medicine 2018 (October 8, 2018): 1–9. http://dx.doi.org/10.1155/2018/4812639.
Full textAbstract:
Longhu Rendan (LHRD), a Chinese traditional compound medicine, has a remarkable treatment effect on motion sickness for about half a century. However, the role of LHRD in atherosclerosis treatment is still unclear. In this study, LHRD treatment significantly diminished total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels in apolipoprotein E gene-knockout (ApoE-/-) mice fed with high fat and high cholesterol diet (western diet). Besides, LHRD treatment significantly reduced atherosclerotic lesion and plaques formation in both aortic roots and aortic trees. Furthermore, immunofluorescence staining in aortic roots demonstrated that LHRD treatment inhibited lectin-like oxidized low-density-lipoprotein receptor-1 (LOX-1) expression in atherosclerotic plaques. These results indicated that LHRD ameliorated atherosclerosis via reducing serum levels of TC, TG, and LDL-C as well as LOX-1 expression, subsequently attenuating atherosclerotic lesion and lipid deposition. In conclusion, LHRD could significantly attenuate experimental atherosclerosis and might be a novel potential drug for the prevention and treatment of atherosclerosis.
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Sun, Changbin, Yahong Fu, Xia Gu, Xiangwen Xi, Xiang Peng, Chuhan Wang, Qi Sun, et al. "Macrophage-Enriched lncRNA RAPIA." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 6 (June 2020): 1464–78. http://dx.doi.org/10.1161/atvbaha.119.313749.
Full textAbstract:
Objective: Despite the current antiatherosclerotic and antithrombotic therapies, the incidence of advanced atherosclerosis-associated clinical events remains high. Whether long noncoding RNAs (lncRNAs) affect the progression of atherosclerosis and whether they are potential targets for the treatment of advanced atherosclerosis are poorly understood. Approach and Results: The progression of atherosclerotic lesions was accompanied by dynamic alterations in lncRNA expression, as revealed by RNA sequencing and quantitative polymerase chain reaction. Among the dynamically changing lncRNAs, we identified a novel lncRNA, lncRNA Associated with the Progression and Intervention of Atherosclerosis (RAPIA), that was highly expressed in advanced atherosclerotic lesions and in macrophages. Inhibition of RAPIA in vivo not only repressed the progression of atherosclerosis but also exerted atheroprotective effects similar to those of atorvastatin on advanced atherosclerotic plaques that had already formed. In vitro assays demonstrated that RAPIA promoted proliferation and reduced apoptosis of macrophages. A molecular sponge interaction between RAPIA and microRNA-183-5p was demonstrated by dual-luciferase reporter and RNA immunoprecipitation assays. Rescue assays indicated that RAPIA functioned at least in part by targeting the microRNA-183-5p/ITGB1 (integrin β1) pathway in macrophages. In addition, the transcription factor FoxO1 (forkhead box O1) could bind to the RAPIA promoter region and facilitate the expression of RAPIA. Conclusions: The progression of atherosclerotic lesions was accompanied by dynamic changes in the expression of lncRNAs. Inhibition of the pivotal lncRNA RAPIA may be a novel preventive and therapeutic strategy for advanced atherosclerosis, especially in patients resistant or intolerant to statins.
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Bekkering, Siroon, Albert P. Limawan, Maria U. Nguyen, Lisa K. Widiasmoko, Hui Lu, Salvatore Pepe, Michael M. Cheung, et al. "Postnatal inflammation following intrauterine inflammation exacerbates the development of atherosclerosis in ApoE−/− mice." Clinical Science 133, no. 10 (May 2019): 1185–96. http://dx.doi.org/10.1042/cs20190141.
Full textAbstract:
Abstract Atherosclerosis is a chronic inflammatory disease that has its origins in early life. Postnatal inflammation exacerbates atherosclerosis, but the possible effect of intrauterine inflammation is largely unexplored. Exposure to inflammation in utero is common, especially in infants born preterm, who have increased cardiovascular risk in adulthood. We hypothesised that exposure to inflammation before birth would accelerate the development of atherosclerosis, with the most severe atherosclerosis following exposure to both pre- and postnatal inflammation. Here we studied the effect of prenatal and postnatal inflammation on the development of atherosclerosis by combining established techniques for modelling histological chorioamnionitis and atherosclerosis using apolipoprotein E (ApoE) knockout mice. A single intra-amniotic (IA) injection of lipopolysaccharide (LPS) caused intrauterine inflammation, and increased atherosclerosis at 13 weeks of postnatal age. In mice exposed to postnatal LPS, chorioamnionitis modulated subsequent responses; atherosclerotic lesion size, number and severity were greatest for mice exposed to both intrauterine and postnatal inflammation, with a concomitant decrease in collagen content and increased inflammation of the atherosclerotic plaque. In conclusion, pre- and postnatal inflammation have additive and deleterious effects on the development of atherosclerosis in ApoE knockout mice. The findings are particularly relevant to preterm human infants, whose gestations are frequently complicated by chorioamnionitis and who are particularly susceptible to repeated postnatal infections. Human and mechanistic studies are warranted to guide preventative strategies.