Journal articles: 'Atherosclerosis – Pathogenesis'

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Crowther, Mark A. "Pathogenesis of Atherosclerosis." Hematology 2005, no. 1 (January 1, 2005): 436–41. http://dx.doi.org/10.1182/asheducation-2005.1.436.

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Abstract Atherosclerosis is no longer considered a disorder due to abnormalities in lipid metabolism. In fact, the inciting event of atherosclerosis is likely an inflammatory insult that occurs decades before the disease becomes clinically apparent. Rapidly evolving knowledge of the pathogenesis of atherosclerosis, coupled with novel, target-specific therapies, is revolutionizing the treatment of atherosclerosis. As a result, a variety of treatments are now undergoing evaluation for their ability to ameliorate the inflammatory pathways likely to cause the atherosclerotic process to initiate and propagate. Once initiated, atherosclerosis progresses as a result of a well-studied series of changes in the constituent cellular make-up of the vessel wall. Specific cytokine-mediated events in this cycle are required for lesional growth. The clinical manifestations of atherosclerosis occur so late in this process that interventions such as percutaneous coronary interventions can deal with isolated areas of disease; however, they do not influence the underlying disease process.

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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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Milioti, Natalia, Alexandra Bermudez-Fajardo, Manuel L. Penichet, and Ernesto Oviedo-Orta. "Antigen-Induced Immunomodulation in the Pathogenesis of Atherosclerosis." Clinical and Developmental Immunology 2008 (2008): 1–15. http://dx.doi.org/10.1155/2008/723539.

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Atherosclerosis is a chronic inflammatory disorder characterised by the accumulation of monocytes/macrophages, smooth muscle cells, and lymphocytes within the arterial wall in response to the release of proinflammatory molecules. Such accumulation results in the formation of the atherosclerotic plaque, which would eventually evolve to complications such as total artery occlusion, rupture, calcification, or aneurysm. Although the molecular mechanism responsible for the development of atherosclerosis is not completely understood, it is clear that the immune system plays a key role in the development of the atherosclerotic plaque and in its complications. There are multiple antigenic stimuli that have been associated with the pathogenesis of atherosclerosis. Most of these stimuli come from modified self-molecules such as oxidised low-density lipoproteins (oxLDLs), beta2glycoprotein1 (2GP1), lipoprotein a (LP(a)), heat shock proteins (HSPs), and protein components of the extracellular matrix such as collagen and fibrinogen in the form of advanced glycation-end (AGE) products. In addition, several foreign antigens including bacteria such as Porphyromonas gingivalis and Chlamydia pneumoniae and viruses such as enterovirus and cytomegalovirus have been associated with atherosclerosis as potentially causative or bystander participants, adding another level of complexity to the analysis of the pathophysiology of atherosclerosis. The present review summarises the most important scientific findings published within the last two decades on the importance of antigens, antigen stimulation, and adaptive immune responses in the development of atherosclerotic plaques.

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Yumino, Dai, and T. Douglas Bradley. "Pathogenesis of Atherosclerosis." American Journal of Respiratory and Critical Care Medicine 176, no. 7 (October 2007): 634–35. http://dx.doi.org/10.1164/rccm.200706-926ed.

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ST. CLAIR, RICHARD W. "Pathogenesis of Atherosclerosis." Cardiology in Review 5, no. 1 (January 1997): 14–24. http://dx.doi.org/10.1097/00045415-199701000-00008.

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Davies, Michael J. "Pathogenesis of atherosclerosis." Current Opinion in Cardiology 7, no. 4 (August 1992): 541–45. http://dx.doi.org/10.1097/00001573-199208000-00002.

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7

KITA, TORU. "Pathogenesis of Atherosclerosis." Japanese Circulation Journal 59, SupplementIII (1995): 828–30. http://dx.doi.org/10.1253/jcj.59.supplementiii_828.

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Consigny, P. M. "Pathogenesis of atherosclerosis." American Journal of Roentgenology 164, no. 3 (March 1995): 553–58. http://dx.doi.org/10.2214/ajr.164.3.7863871.

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Navab, Mohamad, Alan M. Fogelman, Judith A. Berliner, Mary C. Territo, Linda L. Demer, Joy S. Frank, Andrew D. Watson, Peter A. Edwards, and Aidons J. Lusis. "Pathogenesis of atherosclerosis." American Journal of Cardiology 76, no. 9 (September 1995): 18C—23C. http://dx.doi.org/10.1016/s0002-9149(99)80466-4.

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10

Moore, Sean. "Pathogenesis of atherosclerosis." Metabolism 34, no. 12 (December 1985): 13–16. http://dx.doi.org/10.1016/s0026-0495(85)80004-4.

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11

Luoma, J. S., and S. Ylä-Herttuala. "Pathogenesis of atherosclerosis." Pathophysiology 5 (June 1998): 43. http://dx.doi.org/10.1016/s0928-4680(98)80444-6.

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Wang, Tao, and Jagdish Butany. "Pathogenesis of atherosclerosis." Diagnostic Histopathology 23, no. 11 (November 2017): 473–78. http://dx.doi.org/10.1016/j.mpdhp.2017.11.009.

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Falk, Erling. "Pathogenesis of Atherosclerosis." Journal of the American College of Cardiology 47, no. 8 (April 2006): C7—C12. http://dx.doi.org/10.1016/j.jacc.2005.09.068.

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Ylä-Herttuala, Seppo, Jukka Luoma, Hanna Kallionpää, Mikko Laukkanen, Pauliina Lehtolainen, and Helena Viita. "Pathogenesis of atherosclerosis." Maturitas 23 (May 1996): S47—S49. http://dx.doi.org/10.1016/0378-5122(96)01011-0.

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Young, James, Peter Libby, and Uwe Schönbeck. "Cytokines in the Pathogenesis of Atherosclerosis." Thrombosis and Haemostasis 88, no. 10 (2002): 554–67. http://dx.doi.org/10.1055/s-0037-1613256.

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SummaryResearch during the last two decades established atheromatous lesions as active sites of inflammation and immune responses, contrasting to the traditional view of atherosclerosis as an acellular lesion composed of lipid deposits. In particular, cytokines appear to orchestrate the chronic development of atherosclerosis, eventually leading to the formation of complex atherosclerotic plaques, which can trigger acute thromboembolic complications, such as myocardial infarction or stroke. Indeed the rupture-prone plaque, characterized by a thin fibrous cap overlaying a voluminous lipid core, exhibits accumulation of various pro-inflammatory cytokines. These cytokines may control the clinical consequences of plaques by mediating infiltration and accumulation of immunocompetent cells, directing the turnover of fibrillar collagens (governing the fragility of the fibrous cap), or enhancing foam cell formation and thrombogenicity of the lipid core, among other processes outlined in this review. Thus, understanding the role of cytokines in the pathophysiology of the atherosclerotic plaque might provide a promising therapeutic avenue for this prevalent human disease. This review will focus on members of the interleukin, tumor necrosis factor, and interferon families of cytokines in modulating key processes of atherogenesis.

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Nordon, Ian M., Robert J. Hinchliffe, Peter J. Holt, Ian M. Loftus, and Matthew M. Thompson. "Review of Current Theories for Abdominal Aortic Aneurysm Pathogenesis." Vascular 17, no. 5 (January 1, 2009): 253–63. http://dx.doi.org/10.2310/6670.2009.00046.

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Atherosclerotic plaques are a feature of abdominal aortic aneurysms (AAAs). Atherosclerosis and AAA appear to share similar risk factors. These observations have led to the conclusion that AAAs are a consequence of advanced atherosclerosis. This review explores current theories regarding the pathogenesis of AAA and their implications for treatment. A systematic literature search was conducted using the search terms abdominal aortic aneurysm, atherosclerosis, pathogenesis, and systemic disease. Articles were categorized according to the association of AAAs with atherosclerosis, arteriomegaly, peripheral aneurysm, systemic expression, genetics, autoimmunity, oxidative stress, and systemic disease. Twenty-nine articles reporting changes in the systemic vasculature associated with AAA and 12 articles examining the shared risk factor hypothesis were identified. There is insufficient evidence to confirm that AAAs are the result of advanced atherosclerosis. The bulk of evidence points to AAA disease being a systemic disease of the vasculature, with a predetermined genetic susceptibility leading to a phenotype governed by environmental factors.

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Kim, Hyo Soo. "Pathogenesis of Coronary Atherosclerosis." Journal of the Korean Medical Association 45, no. 7 (2002): 860. http://dx.doi.org/10.5124/jkma.2002.45.7.860.

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Douglas, Gillian, and Keith M. Channon. "The pathogenesis of atherosclerosis." Medicine 38, no. 8 (August 2010): 397–402. http://dx.doi.org/10.1016/j.mpmed.2010.05.002.

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Douglas, Gillian, and Keith M. Channon. "The pathogenesis of atherosclerosis." Medicine 42, no. 9 (September 2014): 480–84. http://dx.doi.org/10.1016/j.mpmed.2014.06.011.

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Mahmoudi, Michael. "The pathogenesis of atherosclerosis." Medicine 46, no. 9 (September 2018): 505–8. http://dx.doi.org/10.1016/j.mpmed.2018.06.010.

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Schachter, Michael. "The pathogenesis of atherosclerosis." International Journal of Cardiology 62 (December 1997): S3—S7. http://dx.doi.org/10.1016/s0167-5273(97)00235-0.

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Wang, Tao, Daniel Palucci, Kelsey Law, Bobby Yanagawa, Jennifer Yam, and Jagdish Butany. "Atherosclerosis: pathogenesis and pathology." Diagnostic Histopathology 18, no. 11 (November 2012): 461–67. http://dx.doi.org/10.1016/j.mpdhp.2012.09.004.

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23

Hegele, Robert A. "The pathogenesis of atherosclerosis." Clinica Chimica Acta 246, no. 1-2 (March 1996): 21–38. http://dx.doi.org/10.1016/0009-8981(96)06224-9.

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Gerrity, R. G., and A. S. Antonov. "The pathogenesis of atherosclerosis." Diabetologia 40 (June 20, 1997): S108—S110. http://dx.doi.org/10.1007/s001250051419.

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Fisher, Mark, Laszlo Csiba, Artak Labadzhyan, Jun Zhou, Navneet Narula, and Jagat Narula. "Pathogenesis of intracranial atherosclerosis." Annals of Neurology 72, no. 1 (July 2012): 149. http://dx.doi.org/10.1002/ana.23617.

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Juneja, Manish, Pankaj Raut, Milind Lohkare, and Harshawardhan Dhanraj Ramteke. "Systemic Lupus Erythematosus and Atherosclerosis." Vidarbha Journal of Internal Medicine 32 (August 10, 2022): 129–31. http://dx.doi.org/10.25259/vjim_20_2022.

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Disorders likely ‘inflammatory’ in nature are known to be linked to accelerated atherosclerotic processes that increase the chances of cardiovascular disease. Systemic lupus erythematosus (SLE) is a well-known autoimmune disease for its ability to affect any organ and cause morbidity. One such major cause of morbidity and mortality in SLE is premature coronary heart disease. Inflammation is considered to be the main pathogenesis of atherosclerosis and an important risk factor for vascular disease. Many clinical trials and studies of epidemiological and pathogenesis-related factors revealed that there is a common link between the pathogenesis of autoimmune diseases such as SLE, causing inflammatory responses similar to those seen in atherosclerosis. In the following review article, we will describe how SLE, inflammation and its traditional risk factors, promotes atherosclerosis.

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Gerasimova, Elena V., Tatiana V. Popkova, Daria A. Gerasimova, and Tatiana V. Kirichenko. "Macrophage Dysfunction in Autoimmune Rheumatic Diseases and Atherosclerosis." International Journal of Molecular Sciences 23, no. 9 (April 19, 2022): 4513. http://dx.doi.org/10.3390/ijms23094513.

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One of the problems of modern medical science is cardiovascular pathology caused by atherosclerotic vascular lesions in patients with autoimmune rheumatic diseases (ARDs). The similarity between the mechanisms of the immunopathogenesis of ARD and chronic low-grade inflammation in atherosclerosis draws attention. According to modern concepts, chronic inflammation associated with uncontrolled activation of both innate and acquired immunity plays a fundamental role in all stages of ARDs and atherosclerotic processes. Macrophage monocytes play an important role among the numerous immune cells and mediators involved in the immunopathogenesis of both ARDs and atherosclerosis. An imbalance between M1-like and M2-like macrophages is considered one of the causes of ARDs. The study of a key pathogenetic factor in the development of autoimmune and atherosclerotic inflammation-activated monocyte/macrophages will deepen the knowledge of chronic inflammation pathogenesis.

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Blagov, Alexander V., Alexander M. Markin, Anastasia I. Bogatyreva, Taisiya V. Tolstik, Vasily N. Sukhorukov, and Alexander N. Orekhov. "The Role of Macrophages in the Pathogenesis of Atherosclerosis." Cells 12, no. 4 (February 5, 2023): 522. http://dx.doi.org/10.3390/cells12040522.

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A wide variety of cell populations, including both immune and endothelial cells, participate in the pathogenesis of atherosclerosis. Among these groups, macrophages deserve special attention because different populations of them can have completely different effects on atherogenesis and inflammation in atherosclerosis. In the current review, the significance of different phenotypes of macrophages in the progression or regression of atherosclerosis will be considered, including their ability to become the foam cells and the consequences of this event, as well as their ability to create a pro-inflammatory or anti-inflammatory medium at the site of atherosclerotic lesions as a result of cytokine production. In addition, several therapeutic strategies directed to the modulation of macrophage activity, which can serve as useful ideas for future drug developments, will be considered.

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Kotova, Julia. "The Possible Role of Herpesviruses in the Pathogenesis of Coronary Atherosclerosis." International Journal of Biomedicine 11, no. 4 (December 10, 2021): 391–96. http://dx.doi.org/10.21103/article11(4)_ra1.

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Cardiovascular diseases are still the dominant cause of death worldwide. Coronary artery disease (CAD) is the most common type of heart disease and the leading cause of death for both men and women. Coronary atherosclerosis underlies multiple clinical manifestations ranging from asymptomatic to stable angina, acute coronary syndrome, MI, heart failure, and sudden cardiac death. The prerequisites for a closer study of the pathogenesis of the atherosclerotic process were the development of atherosclerotic vascular lesions at a younger age and the rapid progression of the process. Currently, it is generally accepted that CAD is a multifactorial disease. Attention is drawn to hereditary disorders of the receptor apparatus, endothelial dysfunction, and lipid metabolism disorders. In addition, latent viral infections are one of the etiopathogenetic factors in the development of atherosclerosis. A number of scientific studies have confirmed the relationship between infectious agents and the development of atherosclerotic vascular lesions. The viral etiology of the development and progression of atherosclerosis is the subject of debate among scientists around the world.

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Saranchina, Yu V., S. V. Dutova, O. Yu Kilina, N. V. Khanarin, and T. S. Kulakova. "The role of neutrophils in the pathogenesis of atherosclerosis." Cardiovascular Therapy and Prevention 17, no. 6 (December 20, 2018): 110–16. http://dx.doi.org/10.15829/1728-8800-2018-6-110-116.

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Atherosclerosis (AS) is one of the causes of cardiovascular disease. The formation of atherosclerotic lesions of the arteries is a long process, and clinical symptoms appear already at the stage of atherosclerotic plaque (ASB), which prevents blood flow and can cause coronary heart disease, as well as acute coronary syndrome. The study of atherosclerosis mechanisms at the subclinical level is relevant. This article provides a summary of current data on the structure and functions of neutrophils (NF) in physiological processes. Particular attention is paid to the participation of neutrophils in the damage and formation of vascular endothelial dysfunction. Discusses several mechanisms of involvement of neutrophils in atherogenesis: the production of reactive oxygen species, which cause direct endothelial damage; the synthesis of cytokines that trigger the migration of leukocytes in inflammation; the formation of protein complexes with cholesterol, contributing to their deposition in the vessels, and neutrophil traps, triggering destructive-alterative reactions.

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Suzuki, Kaori, Etsuo A. Susaki, and Isao Nagaoka. "Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis." International Journal of Molecular Sciences 23, no. 19 (September 22, 2022): 11148. http://dx.doi.org/10.3390/ijms231911148.

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Atherosclerosis is a chronic inflammatory disease of the vascular walls related to aging. Thus far, the roles of cellular senescence and bacterial infection in the pathogenesis of atherosclerosis have been speculated to be independent of each other. Some types of macrophages, vascular endothelial cells, and vascular smooth muscle cells are in a senescent state at the sites of atherosclerotic lesions. Likewise, bacterial infections and accumulations of lipopolysaccharide (LPS), an outer-membrane component of Gram-negative bacteria, have also been observed in the atherosclerotic lesions of patients. This review introduces the integration of these two potential pathways in atherosclerosis. Previous studies have suggested that LPS directly induces cellular senescence in cultured monocytes/macrophages and vascular cells. In addition, LPS enhances the inflammatory properties (senescence-associated secretory phenotype [SASP]) of senescent endothelial cells. Thus, LPS derived from Gram-negative bacteria could exaggerate the pathogenesis of atherosclerosis by inducing and enhancing cellular senescence and the SASP-associated inflammatory properties of specific vascular cells in atherosclerotic lesions. This proposed mechanism can provide novel approaches to preventing and treating this common age-related disease.

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Gong, Dong-Mei, Yan-Li Zhang, Dan-Yang Chen, Ling-Juan Hong, Feng Han, Qi-Bing Liu, Jian-Jun Jiang, and Ying-Mei Lu. "Endothelial GPR124 Exaggerates the Pathogenesis of Atherosclerosis by Activating Inflammation." Cellular Physiology and Biochemistry 45, no. 2 (2018): 547–57. http://dx.doi.org/10.1159/000487032.

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Background/Aims: Endothelial cell dysfunction is the principal pathological process underlying atherosclerotic cardiovascular disease. G protein-coupled receptor 124 (GPR124), an orphan receptor in the adhesion GPCR subfamily, promotes angiogenesis in the brain. In the present study, we explored the role of endothelial GPR124 in the development and progression of atherosclerosis in adult mice. Methods: Using tetracycline-inducible transgenic systems, we generated mice expressing GPR124 specifically under control of the Tie-2 promoter. The animal model of atherosclerosis was constructed by intravenously injecting AAV-PCSK9DY into tetracycline-regulated mice and feeding the mice a high-fat diet for 16 consecutive weeks. Biochemical analysis and immunohistochemistry methods were used to address the role and mechanism of GPR124 in the pathological process of atherosclerosis. Results: Higher TC (total cholesterol) and LDL-C (low density lipoprotein cholesterol) levels in serum and greater lipid deposition in the aortic sinus were found in atherosclerotic mice with GPR124 overexpression, coincident with the elevated proliferation of smooth muscle cells. We observed an elevation of ONOO- in the aortic sinus in this model by using immunofluorescence, and the experiments showed that the specific overexpression of GPR124 in the endothelium induced the up-regulation of CD68, NLRP3 and caspase-1 levels in the aortic sinus. Conclusion: The above results indicate that manipulating GPR124 in the endothelium may contribute to delayed pathological progression of atherosclerosis.

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Sarmah, Deepaneeta, Aishika Datta, Swapnil Raut, Ankan Sarkar, Birva Shah, Mariya Bohra, Upasna Singh, et al. "The Role of Inflammasomes in Atherosclerosis and Stroke Pathogenesis." Current Pharmaceutical Design 26, no. 34 (October 13, 2020): 4234–45. http://dx.doi.org/10.2174/1381612826666200427084949.

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Inflammation is a devastating outcome of cerebrovascular diseases (CVD), namely stroke and atherosclerosis. Numerous studies over the decade have shown that inflammasomes play a role in mediating inflammatory reactions post cellular injury occurring after a stroke or a rupture of an atherosclerotic plaque. In view of this, targeting these inflammatory pathways using different pharmacological therapies may improve outcomes in patients with CVD. Here, we review the mechanisms by which inflammasomes drive the pathogenesis of stroke and atherosclerosis. Also, discussed here are the possible treatment strategies available for inhibiting inflammasomes or their up-stream/down-stream mediators.

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Dankevych-Kharchyshyn, Iryna S., Olena M. Vynogradova, Natalia V. Malko, Roman M. Gnid, Andriana P. Skalat, Lidiya Y. Minko, Oleg I. Mrochko, Yurij L. Bandrivsky, and Orysia O. Bandrivska. "PERIODONTAL DISEASES AND ATHEROSCLEROSIS (LITERATURE REVIEW)." Wiadomości Lekarskie 72, no. 3 (2019): 462–65. http://dx.doi.org/10.36740/wlek201903127.

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Introduction: The relationship between periodontal diseases and atherosclerosis is addressed in this article. Both these diseases have an inflammatory basis. Because periodontal disease is a risk factor for developing atherosclerotic vascular disease, diagnosis of the former is important. Particular attention must be paid to patients who have periodontal disease with other risk factors for atherosclerotic vascular disease. Recommendations managing these patients have been made included. The aim: The paper is aimed at familiarization of broad medical public with the presence of the relationship between diseases of periodontal tissues and atherosclerosis. Materials and methods: A thorough comprehensive analysis and generalization of scientific achievements elucidated in the fundamental and periodical publications, relating to diseases of the periodontal tissues and atherosclerosis, has been carried out. Review: The article consists of many researchers regarding the prevalence and intensity of periodontal tissue diseases in people of all ages. Problems associated with the state of periodontal tissues in people under study as dentists and general practitioners. Proven role in the pathogenesis of inflammatory diseases of the periodontal tissues in people with atherosclerosis. In the modern concept of the etiology and pathogenesis of periodontal diseases in people is extremely important role for the immune system and resistance to periodontal bacterial invasion. Analyzed common changes important for pathogenesis of periodontal tissue diseases and atherosclerosis. Conclusions: Consequently, recent studies have shown a clear, directly proportional relationship between periodontal tissue diseases and atherosclerosis, but mechanisms for their development and interaction are not fully disclosed.

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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.

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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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SHIMIZU, Nobuya, Yoshihito SATO, Akihiko TAMURA, Hideyo KATSUNUMA, and Yoshiyuki SEYAMA. "Pathogenesis of Atherosclerosis and Elastin." Journal of Japan Atherosclerosis Society 14, no. 5 (1986): 1027–32. http://dx.doi.org/10.5551/jat1973.14.5_1027.

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Kazymyrko, V. K., L. M. Ivanitska, T. S. Silantieva, and V. V. Kutovyi. "UNIVERSAL THEORY OF ATHEROSCLEROSIS PATHOGENESIS." Likarska sprava, no. 7-8 (December 31, 2019): 3–12. http://dx.doi.org/10.31640/jvd.7-8.2019(1).

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The paper shows that atherosclerosis results from disturbed cholesterol homeostasis in the body, the development of systemic stromal-vascular lipid-protein dystrophy (or lipidosis, or cholesterolosis) complicated by extracellular focal lipid deposits with a predominant cholesterol in the interstitial tissue of the inner arterial and aortic layer. These deposits are foreign to this body tissue. They induce the development of chronic productive granulomatous inflammation in it – granulomatosis around endogenous foreign bodies. Cholesterol deposition is promoted by a positive cholesterol balance in the body; increased permeability of the endothelium in hemodynamically vulnerable parts of the arteries, where blood components, including LP, infiltrate their wall; a lack of hydrolytic enzymes in the cell lysosomes that could destroy the steroid nucleus of the cholesterol molecule. Being essential for each specific organism (for building membranes, the formation of bile acids, the synthesis of steroid hormones, vitamin D3), cholesterol, if exceeded, can increase the probability of developing atherosclerosis. Genetic mechanisms are implicated in the disturbed lipid protein metabolism in the human body. Hyperlipoproteinemias (HLPs) are known to be the most common metabolic disorders. The dystrophy under consideration results from primary HLP types IIa, IIb, III, IV, V, as well as secondary HLPs in patients with various medical conditions associated with an increase in blood LDL and / or VLDL and/or a decrease in HDL. A reduced cholesterol efflux from peripheral tissues due to a decreased HDL content and the development of lipidosis are seen in diabetes, obesity, physical inactivity, stress, puberty, menopause, hypertriglyceridemia, cigarette smoking, uremia, treatment with anabolic steroids, beta-adrenergic blocking agents, gestagens, and the use of contraceptives. The most pronounced manifestations of dystrophy are characteristic of HLP types IIA, IIb, III, but its moderate development complicated by atherosclerosis also occurs in types IV and V, which are accompanied by increased blood VLDL. Mutations of LDL receptor genes, apoprotein genes lead to the development of stromal vascular dystrophy and atherosclerosis. A number of rare genetic disorders of sterol metabolism accompany impaired metabolism of cholesterol and its esters: hepatic lipase deficiency (with accumulation of VLDL and IDLs); a deficiency in lysosomal hydrolase of cholesterol esters with impaired LDL metabolism (Wolman disease); cholesterol ester accumulation disease; cerebrotendinous xanthomatosis; cerebral cholesterolosis; Toichlander and Hand Schüler Christian syndromes. The main factor contributing to the development of inflammation in the inner vascular wall of arteries and aorta in atherosclerosis is the cyclic hydrocarbonic structure of cholesterol, which cannot be cleaved in the lysosomes of MPs. The leading role of the cyclic hydrocarbonic structure of cholesterol, which is insoluble and indestructible by MPs, in the induction of atherosclerosis-related inflammation is confirmed by the fact of the atherogenic action of cholesterol derivatives having its structure. An important factor in inflammatory morphogenesis is the lipoprotein dyscolloidosis occurring in the arterial intima and the physical and chemical metamorphosis of cholesterol. A colloidal solution, solid crystals of free cholesterol and liquid crystals of cholesterol esters have a pronounced phlogogenic and sclerogenic effect on the interstitial tissue of the arterial intima.

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Kaehler, J., S. Osterholz, M. Patten, R. Koester, and T. Meinertz. "Cytokines in pathogenesis of atherosclerosis." DMW - Deutsche Medizinische Wochenschrift 127, no. 3 (2002): 94–99. http://dx.doi.org/10.1055/s-2002-19597.

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Doronin, A. A., V. A. Pavlina, L. V. Sivakova, and I. L. Gulyaeva. "ETIOLOGY AND PATHOGENESIS OF ATHEROSCLEROSIS." European Journal of Natural History, no. 4 2022 (2022): 31–35. http://dx.doi.org/10.17513/ejnh.34285.

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Gotlieb, Avrum I., and Peter Anderson. "Atherosclerosis: New insights into pathogenesis." Cardiovascular Pathology 1, no. 4 (October 1992): 243–44. http://dx.doi.org/10.1016/1054-8807(92)90033-k.

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Kimura, Yoshitaka, Daisuke Tsukui, and Hajime Kono. "Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis." International Journal of Molecular Sciences 22, no. 22 (November 17, 2021): 12394. http://dx.doi.org/10.3390/ijms222212394.

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Hyperuricemia is a common metabolic syndrome. Elevated uric acid levels are risk factors for gout, hypertension, and chronic kidney diseases. Furthermore, various epidemiological studies have also demonstrated an association between cardiovascular risks and hyperuricemia. In hyperuricemia, reactive oxygen species (ROS) are produced simultaneously with the formation of uric acid by xanthine oxidases. Intracellular uric acid has also been reported to promote the production of ROS. The ROS and the intracellular uric acid itself regulate several intracellular signaling pathways, and alterations in these pathways may result in the development of atherosclerotic lesions. In this review, we describe the effect of uric acid on various molecular signals and the potential mechanisms of atherosclerosis development in hyperuricemia. Furthermore, we discuss the efficacy of treatments for hyperuricemia to protect against the development of atherosclerosis.

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Spartalis, Michael, Eleftherios Spartalis, Antonios Athanasiou, Stavroula A. Paschou, Christos Kontogiannis, Georgios Georgiopoulos, Dimitrios C. Iliopoulos, and Vassilis Voudris. "The Role of the Endothelium in Premature Atherosclerosis: Molecular Mechanisms." Current Medicinal Chemistry 27, no. 7 (March 16, 2020): 1041–51. http://dx.doi.org/10.2174/0929867326666190911141951.

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Atherosclerotic disease is still one of the leading causes of mortality. Atherosclerosis is a complex progressive and systematic artery disease that involves the intima of the large and middle artery vessels. The inflammation has a key role in the pathophysiological process of the disease and the infiltration of the intima from monocytes, macrophages and T-lymphocytes combined with endothelial dysfunction and accumulated oxidized low-density lipoprotein (LDL) are the main findings of atherogenesis. The development of atherosclerosis involves multiple genetic and environmental factors. Although a large number of genes, genetic polymorphisms, and susceptible loci have been identified in chromosomal regions associated with atherosclerosis, it is the epigenetic process that regulates the chromosomal organization and genetic expression that plays a critical role in the pathogenesis of atherosclerosis. Despite the positive progress made in understanding the pathogenesis of atherosclerosis, the knowledge about the disease remains scarce.

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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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Orecchioni, Marco, Kouji Kobiyama, Holger Winkels, Yanal Ghosheh, Sara McArdle, Zbigniew Mikulski, William B. Kiosses, et al. "Olfactory receptor 2 in vascular macrophages drives atherosclerosis by NLRP3-dependent IL-1 production." Science 375, no. 6577 (January 14, 2022): 214–21. http://dx.doi.org/10.1126/science.abg3067.

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Sniffing out atherosclerosis Olfactory receptors are best known for their presence in the nose and their role in detecting smells, but they are also present in other tissues and perform additional biological functions. For example, vascular macrophages involved in the pathogenesis of atherosclerosis express multiple subtypes of olfactory receptors. Orecchioni et al . focused on olfactory receptor 2, a receptor for the compound octanal, and identified its contribution to atherosclerosis pathogenesis and the formation of atherosclerotic plaques (see the Perspective by Rayner and Rasheed). The authors show that most of the octanal was not directly derived from the diet, but rather was generated as a by-product of lipid peroxidation, suggesting a potential pathway for intervention. —YN

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Paszek, Elżbieta, Wojciech Zajdel, Tomasz Rajs, Krzysztof Żmudka, Jacek Legutko, and Paweł Kleczyński. "Profilin 1 and Mitochondria—Partners in the Pathogenesis of Coronary Artery Disease?" International Journal of Molecular Sciences 22, no. 3 (January 22, 2021): 1100. http://dx.doi.org/10.3390/ijms22031100.

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Atherosclerosis remains a large health and economic burden. Even though it has been studied for more than a century, its complex pathophysiology has not been elucidated. The relatively well-established contributors include: chronic inflammation in response to oxidized cholesterol, reactive oxygen species-induced damage and apoptosis. Recently, profilin 1, a regulator of actin dynamics emerged as a potential new player in the field. Profilin is abundant in stable atherosclerotic plaques and in thrombi extracted from infarct-related arteries in patients with acute myocardial infarction. The exact role of profilin in atherosclerosis and its complications, as well as its mechanisms of action, remain unknown. Here, we summarize several pathways in which profilin may act through mitochondria in a number of processes implicated in atherosclerosis.

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Ciccarelli, Giovanni, Stefano Conte, Giovanni Cimmino, Patrizia Maiorano, Andrea Morrione, and Antonio Giordano. "Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?" International Journal of Molecular Sciences 24, no. 2 (January 6, 2023): 1086. http://dx.doi.org/10.3390/ijms24021086.

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Atherosclerosis is a multifactorial inflammatory pathology that involves metabolic processes. Improvements in therapy have drastically reduced the prognosis of cardiovascular disease. Nevertheless, a significant residual risk is still relevant, and is related to unmet therapeutic targets. Endothelial dysfunction and lipid infiltration are the primary causes of atherosclerotic plaque progression. In this contest, mitochondrial dysfunction can affect arterial wall cells, in particular macrophages, smooth muscle cells, lymphocytes, and endothelial cells, causing an increase in reactive oxygen species (ROS), leading to oxidative stress, chronic inflammation, and intracellular lipid deposition. The detection and characterization of mitochondrial DNA (mtDNA) is crucial for assessing mitochondrial defects and should be considered the goal for new future therapeutic interventions. In this review, we will focus on a new idea, based on the analysis of data from many research groups, namely the link between mitochondrial impairment and endothelial dysfunction and, in particular, its effect on atherosclerosis and aging. Therefore, we discuss known and novel mitochondria-targeting therapies in the contest of atherosclerosis.

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Dong, Yunzhou, Conrad Fernandes, Yanjun Liu, Yong Wu, Hao Wu, Megan L. Brophy, Lin Deng, et al. "Role of endoplasmic reticulum stress signalling in diabetic endothelial dysfunction and atherosclerosis." Diabetes and Vascular Disease Research 14, no. 1 (October 20, 2016): 14–23. http://dx.doi.org/10.1177/1479164116666762.

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It is well established that diabetes mellitus accelerates atherosclerotic vascular disease. Endothelial injury has been proposed to be the initial event in the pathogenesis of atherosclerosis. Endothelium not only acts as a semi-selective barrier but also serves physiological and metabolic functions. Diabetes or high glucose in circulation triggers a series of intracellular responses and organ damage such as endothelial dysfunction and apoptosis. One such response is high glucose-induced chronic endoplasmic reticulum stress in the endothelium. The unfolded protein response is an acute reaction that enables cells to overcome endoplasmic reticulum stress. However, when chronically persistent, endoplasmic reticulum stress response could ultimately lead to endothelial dysfunction and atherosclerosis. Herein, we discuss the scientific advances in understanding endoplasmic reticulum stress-induced endothelial dysfunction, the pathogenesis of diabetes-accelerated atherosclerosis and endoplasmic reticulum stress as a potential target in therapies for diabetic atherosclerosis.

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Sazonova, Margarita A., Vasily V. Sinyov, Anastasia I. Ryzhkova, Elena V. Galitsyna, Zukhra B. Khasanova, Anton Yu Postnov, Elena I. Yarygina, Alexander N. Orekhov, and Igor A. Sobenin. "Role of Mitochondrial Genome Mutations in Pathogenesis of Carotid Atherosclerosis." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/6934394.

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Mutations of mtDNA, due to their higher frequency of occurrence compared to nuclear DNA mutations, are the most promising biomarkers for assessing predisposition of the occurrence and development of atherogenesis. The aim of the present article was an analysis of correlation of several mitochondrial genome mutations with carotid atherosclerosis. Leukocytes from blood of study participants from Moscow polyclinics were used as research material. The sample size was 700 people. The sample members were diagnosed with “atherosclerosis” on the basis of ultrasonographic examination and biochemical and molecular cell tests. DNA was isolated from blood leukocyte samples of the study participants. PCR fragments of DNA, containing the region of 11 investigated mutations, were pyrosequenced. The heteroplasmy level of these mutations was detected. Statistical analysis of the obtained results was performed using the software package SPSS 22.0. According to the obtained results, an association of mutations m.652delG, m.3336C>T, m.12315G>A, m.14459G>A m.15059G>A with carotid atherosclerosis was found. These mutations can be biomarkers for assessing predisposition to this disease. Additionally, two single nucleotide substitutions (m.13513G>A and m.14846G>A), negatively correlating with atherosclerotic lesions, were detected. These mutations may be potential candidates for gene therapy of atherosclerosis and its risk factors.

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Singla, Sandeep, Changping Hu, Adam Mizeracki, and Jawahar L. Mehta. "Decorin in atherosclerosis." Therapeutic Advances in Cardiovascular Disease 5, no. 6 (November 16, 2011): 305–14. http://dx.doi.org/10.1177/1753944711429715.

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Atherosclerotic cardiovascular disease is a major cause of morbidity and mortality in the Western world. Despite tremendous strides in understandings its pathogenesis, it still remains a challenge because of gaps in our understanding of its initiation, progression and complications leading to the clinical syndromes of angina, acute coronary syndrome, cerebrovascular disease and peripheral vascular disease. Recent studies have provided impetus on the shift from models of atherosclerosis based on cellular interactions to models where the important role of extracellular matrix is recognized. Proteoglycans, especially those belonging to the small leucine-rich proteoglycan family of which decorin is a representative example, have come under close scrutiny for their role in atherogenesis. There is evidence from in vitro and in vivo animal models as well as humans to suggest an important role of decorin in attenuating progression of atherosclerosis. Decorin distribution in different blood vessels has been shown to inversely correlate with the tendency to develop atherosclerosis. Decorin seems to interact closely with different cellular components of the plaque milieu, thereby suggesting its role in influencing atherogenesis at different steps. Here we review the current understanding of the role of decorin in the pathogenesis of atherosclerosis.

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Journal articles on the topic 'Atherosclerosis – Pathogenesis'

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