Relevant bibliographies by topics / Atherosclerosis – Pathogenesis

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Atherosclerosis – Pathogenesis'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "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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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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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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Dissertations / Theses on the topic "Atherosclerosis – Pathogenesis"

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Kelly, Ann Kelly Ann. "C-Myb in the pathogenesis of atherosclerosis." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502268.

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C-Myb is a DNA-binding transcription factor that functions in apoptosis, proliferation and differentiation. The role of c-Myb in vascular injury has been investigated in vitro and in vivo. Knock-down of c-Myb leads to a reduction in proliferation and an increase in apoptosis in vascular smooth muscle cells (VSMCs). Reduction of c-Myb activity has also been shown to reduce the incidence of neointimal formation in vivo by reducing VSMC proliferation. In contrast, over-expression of c-Myb in vivo leads to increased survival rates in certain cell types. Despite these observations, c-Myb expression has not yet been investigated in atherosclerosis. The balance between apoptosis and proliferation is pivotal in the pathogenesis of the disease. The aim of this thesis w as to investigate c-Myb expression in atherosclerotic lesions in addition to elucidating possible mechanisms by which c-Myb functions in atherosclerosis.
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Wilson, Stephanie Helen. "Pathogenesis and treatment of cholesterol-related early vascular injury." Thesis, The University of Sydney, 2000. https://hdl.handle.net/2123/28453.

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This thesis describes studies into the pathogenesis of Cholesterol—related early vascular injury. In addition, this thesis examines the potential reversibility of this injury with 2 agents: a) simvastatin, an HMGCoA reductase inhibitor, in a model independent of any reduction in lipids and 2) high dose aspirin. Hypercholesterolaemia led to a decrease in NO bioavailability, in association with a decrease in the enzyme, endothelial nitric oxide synthase and increased oxidative stress. In addition, there was an increase in the pro—inflammatory transcription factor, NF—KB, in the intima of the epicardial coronary arteries. Moreover, activated NF—KB was present in macrophages, foam cells and vascular smooth muscle cells in coronary atheromatous plaque and its expression increased in unstable coronary syndromes. These data support a role for NF—KB in the pathogenesis of early atherosclerosis and the development of unstable coronary syndromes. In addition, this thesis demonstrated for the first time that simvastatin, an HMGCoA reductase inhibitor, preserves endothelium—dependent vasorelaxation in both large and small coronary vessels in porcine experimental HC, despite no reduction in plasma lipids. This effect was associated with normalisation of eNOS protein levels. Furthermore, in vivo plasma markers of oxidative stress were attenuated by treatment with simvastatin. However, there was no attenuation in the activation of the proinflammatory transcription factor, NF—KB. These studies suggest a role for the HMGCoA reductase inhibitors in reducing cardiac morbidity and mortality, beyond their effect on cholesterol levels. The current studies also demonstrated that high dose aspirin therapy preserved endothelial function in large coronary vessels. This alteration in the generation of prostanoids in favour of vasodilatation may be an important component of the therapeutic benefit of aspirin in HC-induced atherosclerosis. In summary, results of studies described in this thesis provide insights into the molecular mechanisms that may be responsible for early vascular injury in hypercholesterolaemia and its reversibility with the therapeutic agents, simvastatin and high dose aspirin.
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McAllister, Andrew Samuel. "Studies of endothelial function in relation to the pathogenesis of atherosclerosis." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387897.

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James, Nicola Jane. "Cellular signalling by tissue factor and lipoproteins in the pathogenesis of atherosclerosis." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246306.

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Lee, Wai Kwong. "Advanced glycosylation endproducts in the pathogenesis of the late complications of diabetes and atherosclerosis." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318168.

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Romo, Saladrigas Neus. "Innate response to human cytomegalovirus and the role of infections in the pathogenesis of atherosclerosis." Doctoral thesis, Universitat Pompeu Fabra, 2011. http://hdl.handle.net/10803/78874.

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We comparatively analyzed the natural killer (NK) cell response against HCMV-infected pro-inflammatory (M1) and anti-inflammatory (M2) M[Fi] derived from autologous monocytes. M1 M[Fi] were more resistant to infection, secreting TNF-[alfa], IL-6, IL-12 and type I IFN. By contrast, in HCMV-infected M2 M[Fi] the production of proinflammatory cytokines, type I IFN and IL-10 was limited, and IL-12 undetectable. NK cell degranulation was triggered by interaction with HCMV-infected M1 and M2 M[Fi] and was partially inhibited by specific anti-NKp46, anti-DNAM-1 and anti-2B4 mAbs, thus supporting a dominant role of these activating receptors. By contrast, only HCMV-infected M1 M[Fi] efficiently promoted NK cell-mediated IFN-[gamma] secretion, an effect partially related to IL-12 production. These observations reveal differences in the NK cell response triggered by distinct HCMV-infected monocyte-derived cell types, which may be relevant in the pathogenesis of this viral infection. HCMV infection has been proposed to contribute to the development of atherosclerosis, a chronic inflammatory process in which M[Fi] play a key role. The contribution of HCMV to vascular disease may depend on features of the immune response not reflected by the detection of specific antibodies. Persistent HCMV infection in healthy blood donors has been associated with changes in the distribution of NK cell receptors (NKR). The putative relationship among HCMV infection, NKR distribution, subclinical atherosclerosis and coronary heart disease was assessed. An association of overt and subclinical atherosclerotic disease with LILRB1+ NK and T cells was observed, likely reflecting a relationship between the immune challenge by infections and cardiovascular disease risk, without attributing a dominant role for HCMV.
Hem analitzat la resposta de la cèl•lula NK als macròfags proinflamatoris (M1) i antiinflamatoris (M2) derivats de monòcits autòlegs infectats pel citomegalovirus humà (HCMV). Els macròfags M1 son més reistents a la infecció i secreten TNF-[alfa], IL-6, IL-12 i IFN de tipus I. Per altra banda, en els macròfags M2 infectats per HCMV la producció de citoquines proinflamatories, IFN de tipus I i IL-10 es limitada i la IL-12 indetectable. La cèl•lula NK degranula al interaccionar amb els macròfags M1 i M2 infectats. Aquesta degranulació s’inhibeix parcialment al bloquejar amb anticossos específics anti-NKp46, anti-DNAM-1 i anti-2B4, això indica que aquests receptors tenen un rol important en el procés. En canvi, només els macròfags M1 infectats amb HCMV promouen de manera eficient la producció d’IFN-[gamma] per part de la cèl•lula NK, degut parcialment a la producció de IL-12. Aquestes observacions posen de manifest diferències en la resposta de la cèl•lula NK a diferents tipus de macròfags infectats per HCMV que pot ser relevant en la patogènesis d’aquesta infecció viral. S’ha proposat que la infecció per HCMV contribueix al desenvolupament de l’aterosclerosis, un procés inflamatori crònic en el que els macròfags tenen un paper clau. La contribució del HCMV a la malaltia cardiovascular pot dependre de la resposta immune. La infecció per HCMV en donants de sang sans s’ha associat a canvis en la distribució dels receptors de les cèl•lules NK. S’ha evaluat la possible relació entre la infecció per HCMV, la distribució dels receptors de les cèl•lules NK i l’infart agut de miocardi. S’ha observat una associació de l’infart agut de miocardi i l’aterosclerosi subclínica tant amb les cèl•lules NK LILRB1+ com amb les cèl•lules T LILRB1+. Això possiblement reflexa la relació entre la pressió que les infeccions exerceixen en el sistema immunitari i el risc cardiovascular sense atribuir un paper principal al HCMV.
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Cao, Fei. "Chlamydia pneumoniae, toll-like receptors and pathogenesis of atherosclerotic heart disease." View the abstract Download the full-text PDF version (on campus access only), 2007. http://etd.utmem.edu/ABSTRACTS/2007-022-Cao-index.html.

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Thesis (Ph.D. )--University of Tennessee Health Science Center, 2007.
Title from title page screen (viewed on May 16, 2008 ). Research advisor: Gerald I. Byrne, Ph.D. Document formatted into pages (xi, 114 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 65-107).
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Dane-Stewart, Cheryl Ann. "Postprandial lipoprotein metabolism in patients at high risk of coronary artery disease : effects of statin therapy." University of Western Australia. School of Medicine and Pharmacology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0061.

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[Formulae and special characters can only be approximated here. Please see the pdf version of the abstract for an accurate reproduction.] Atherosclerosis is a common degenerative disease in which the clinical manifestations are often through stroke or myocardial infarction. Some of the established risk factors for atherosclerosis include elevated plasma low-density lipoprotein (LDL)-cholesterol levels, obesity, diabetes mellitus (DM) and cigarette smoking. Of the risk factors, an elevation in plasma LDL is one of the most established and the most researched. This is partly a consequence of the deposition of cholesterol within arterial intima being a crucial step in the progression of atherosclerosis, combined with the finding that LDL particles are a major transporter of cholesterol in circulation. Recently there is increasing evidence showing a role of the other major transporter of cholesterol in circulation, chylomicron remnants, in the progression of atherosclerosis. The notion of atherosclerosis as a postprandial phenomenon has been further substantiated by the emergence of evidence showing a direct role of chylomicron remnants in arterial cholesterol deposition. Based on evidence that chylomicron remnants are proatherogenic, the suggestion arises that accumulation of postprandial lipoproteins in plasma may add another dimension of risk to the development of coronary artery disease (CAD). This thesis tests the general hypothesis that individuals with or at high risk of CAD have postprandial dyslipidaemia and that this metabolic abnormality is correctable with a class of lipid-lowering drugs called statins. To test the hypothesis, clinical studies were conducted in normolipidaemic CAD patients, heterozygous familial hypercholesterolaemia (FH) and postmenopausal women with type 2 DM. Determination of postprandial dyslipidaemia by comparison with control populations were conducted initially in each patient group (Studies 1, 3 and 5), followed by intervention studies investigating possible modulation of the dyslipidaemia with a statin (Studies 2, 4 and 6). Six observation statements based on case-control comparisons of postprandial lipaemia in patients with or at risk of CAD and the effects of statins on postprandial dyslipidaemia in the patient groups were derived from the general hypothesis. The observation statements were examined in the individual studies described below. Postprandial lipoprotein metabolism was assessed using a number of methods. For comparison of postprandial lipaemia in Studies 1 and 2, a classic oral fat challenge was utilised. As markers of chylomicrons and chylomicron remnants, retinyl palmitate and triglyceride were measured postprandially as well as apolipoprotein (apo) B48 concentrations, a specific marker of intestinal lipoproteins. ApoB48 was also measured in the fasting state and found to predict the postprandial responses of retinyl palmitate, triglyceride and apoB48. This suggested that fasting measurement of apoB48 could be used as a simple indicator of postprandial dyslipidaemia. Consequently for Studies 3 - 6, fasting apoB48 measurements were used as primary markers of postprandial dyslipidaemia. Other markers for chylomicrons and their remnants utilised were fasting plasma concentrations of remnant-like particle-cholesterol (RLP-C) and apoC-III. As well as these static markers, chylomicron remnant catabolism was measured using a stable isotope breath test. The breath test involves the intravenous injection of a chylomicron remnant-like emulsion labelled with ¹³C-oleate and measurement of enriched ¹³CO2 in expired breath by isotope ratio mass spectrometry. The fractional catabolic rate (FCR) of the injected emulsion was subsequently calculated using multi-compartmental modeling (SAAM II). The studies are presented in this thesis as published and unpublished works. In Study 1, postprandial lipoprotein metabolism was compared between 18 normolipidaemic CAD patients (cholesterol 4.54 ± 0.12 mmol/L, triglyceride 1.09 ± 0.16) with 13 asymptomatic healthy controls using an oral fat challenge. Normolipidaemic CAD patients had higher postprandial area-under-curve (AUC) for triglyceride (+34%, p=0.019), retinyl palmitate (+74%, p=0.032) and apoB48 (+36%, p<0.001). Fasting apoB48 was also higher (+41%, p=0.001) and found to correlate significantly with AUC of triglyceride (p=0.017), retinyl palmitate (p=0.001) and apoB48 (p<0.001). The data suggest that normolipidaemic CAD patients have increased concentrations of intestinal lipoproteins in the fasting and postprandial state. In addition to these findings, significant correlations of fasting apoB48 with postprandial markers (p<0.02) suggests the fasting marker to be a simpler surrogate marker for the degree of total postprandial lipaemia. Study 2 investigated the effect of atorvastatin treatment on postprandial dyslipidaemia found in the 18 near-normolipidaemic CAD patients from Study 1. The trial was conducted in a randomised, placebo-controlled design, using oral fat challenges before and after 12-weeks atorvastatin/placebo treatment. Compared with the placebo group, atorvastatin decreased the total postprandial AUC for iii triglyceride (-22%, p=0.05) and apoB48 (-34%, p=0.013). Fasting markers of apoB48 (-35%, p=0.019) and RLP-C (-36%, p=0.032) also decreased significantly. Atorvastatin was also found to increase LDL-receptor activity by +218% (p<0.001) as reflected in binding studies. The data suggest atorvastatin reduces the fasting levels of intestinal lipoproteins as well as total postprandial lipaemia, but without acute dynamic changes in postprandial lipaemia. The reduction in fasting and total postprandial lipoprotein levels could be partly attributed to an increase in LDL-receptor mediated removal from circulation. In Study 3, postprandial lipaemia was compared in 15 heterozygous FH patients with 15 healthy controls. FH patients had higher fasting concentrations of apoB48 (+56%, p<0.001) and RLP-C (+48%, p=0.003). The elevation in these fasting markers of chylomicrons and their remnants suggests FH patients have postprandial dyslipidaemia due to an accumulation of these particles in plasma. Study 4 examined the effects of long- (> 6 months) and short-term (4 weeks) simvastatin treatment on modulating postprandial dyslipidaemia found in the 15 FH patients from Study 3. Short- and long-term simvastatin treatment decreased the fasting concentrations of apoB48 (-29% and 15% respectively, p<0.05) and RLP-C (both -38%, p<0.001), but did not significantly alter the FCR of the injected chylomicron remnant-like emulsion. The data suggest that in heterozygous FH both long- and short-term simvastatin treatments decrease the fasting markers of postprandial lipoproteins by mechanisms that may not be mediated via processes differentiated by the 13CO2 breath test. This implies that the effect on postprandial lipaemia may be from a decrease in production and/or a possible increase in catabolism of triglyceride-rich lipoproteins (TRLs). In Study 5, postprandial lipaemia was compared in 24 postmenopausal women age and body mass index matched with 14 postmenopausal women with type 2 DM. Postmenopausal diabetic women were found to have higher fasting concentrations of apoB48 (+21%, p=0.021) and apoC-III (+16%, p=0.042) as well as lower FCR of the chylomicron remnant-like emulsion (-50%, p<0.001). The data suggest that postmenopausal diabetic women have postprandial dyslipidaemia, and that this is due to delayed catabolism of chylomicron remnants. Study 6 was an hypothesis-generating exercise examining the effects of 4-weeks pravastatin treatment on postprandial dyslipidaemia found in 7 postmenopausal women with type 2 DM from Study 5. Although plasma LDL-cholesterol was reduced (-19%, p=0.028), there were no significant effects found on fasting apoB48 concentrations (-12%, p=0.116) or the FCR of the chylomicron remnant-like emulsion (+38%, p=0.345). A larger sample size of patients and/or treatment with a more potent statin at a dosage known to affect chylomicron remnant metabolism would be required to demonstrate a significant reduction in postprandial dyslipidaemia in postmenopausal women with type 2 DM. The results of the above mentioned studies combined support the general hypothesis that postprandial dyslipidaemia is a feature of patients with or at risk of CAD. This defect may be demonstrated using fasting apoB48 as an indicator of the degree of postprandial lipaemia. Postprandial dyslipidaemia may reflect a reduction in catabolism, as suggested with the breath test in type 2 DM, and/or an over overproduction of chylomicrons. Both these mechanisms would also increase competition for lipolysis and clearance pathways between hepatically and intestinally-derived lipoproteins. The exact mechanisms by which postprandial dyslipidaemia occurs are yet to be determined. Statins appear to improve defective postprandial lipaemia in patients with or at risk of CAD, which is in agreement with the general hypothesis. The effectiveness of a statin is dependant on their potency in inhibiting cholesterol biosynthesis and increasing receptor mediated clearance of LDL and chylomicron remnants. The studies conducted in this thesis show that postprandial dyslipidaemia can be reduced by statins but not to the extent demonstrated in controls. However, the demonstrated reduction in fasting and total postprandial lipaemia translates to a lowering in overall arterial exposure to circulating proatherogenic particles. The elevation in fasting and postprandial levels of proatherogenic chylomicron remnants found in the patient groups described in this thesis indicates another dimension to their risk of coronary disease. The reductions in the overall levels of proatherogenic particles in patients with or at high CAD risk, infers a possible reduction in the risk of coronary disease in these patients.
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Rygelski, Marian Mikaela, and Marian Mikaela Rygelski. "The Role of Inflammation in Cardiovascular Disease in HIV-Infected Patients." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/626402.

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Human Immunodeficiency Virus Type I, or HIV, is one of the most well-known and well-researched viruses in the world. The current standard of care for HIV infected individuals is an antiretroviral drug therapy regiment, or ART, started immediately after diagnosis. While this treatment is generally quite effective at keeping the viral load low and stopping the progression from HIV infection to AIDS, patients receiving ART therapy still have a lower life expectancy than uninfected individuals. Many times, the cause of death in these patients is not the common opportunistic pathogens and cancers linked to HIV and AIDS, but chronic health conditions that develop. One of these conditions that is seen in many of the HIV infected patients undergoing the antiretroviral therapy is cardiovascular disease, such as atherosclerosis and myocardial infarction. Research shows that one of the key players in developing these conditions in HIV patients is the chronic inflammation caused by the immune system attempts to control the level of the virus. By studying the links between HIV, inflammation, and cardiovascular disease, we may be able to find solutions to the development of chronic disease in HIV patients on antiretroviral therapy.
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Ledford, Kelly J. "Loss of CEACAM1 in the Pathogenesis of Vascular Abnormalities Associated with the Metabolic Syndrome." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1271345465.

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Books on the topic "Atherosclerosis – Pathogenesis"

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Haverich, Axel, and Erin Colleen Boyle. Atherosclerosis Pathogenesis and Microvascular Dysfunction. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-20245-3.

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Modified lipoproteins in the pathogenesis of atherosclerosis. Austin: R.G. Landes Co., 1994.

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Subbiah, M. T. R., 1942-, ed. Atherosclerosis: A pediatric perspective. Boca Raton, Fla: CRC Press, 1989.

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N, Diana John, ed. Tobacco smoking and atherosclerosis: Pathogenesis and cellular mechanisms. New York: Plenum Press, 1990.

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L, Malmendier Claude, and Alaupovic P, eds. Eicosanoids, apolipoproteins, lipoprotein particles, and atherosclerosis. New York: Plenum, 1988.

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1944-, Shepherd J., Packard Christopher J, and Brownlie Sheena M, eds. Lipoproteins and the pathogenesis of atherosclerosis: Proceedings of the International Symposium on Lipoproteins and the Pathogenesis of Atherosclerosis, Gleneagles, Perthshire, 24-27 February 1991. Amsterdam: Excerpta Medica, 1991.

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Workshop on Carotid Artery Plaques (1987 Gutersloh, Germany). Carotid artery plaques: Pathogenesis, development, evaluation, treatment. Edited by Hennerici M, Sitzer G, Weger Hans-Dieter, Bertelsmann Stiftung (Gütersloh Germany), and Universität Düsseldorf. Dept. of Neurology. Basel: Karger, 1988.

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P, Gallos Alice, and Jones Margaret L, eds. Angina pectoris: Etiology, pathogenesis, and treatment. New York: Nova Science Publishers, 2008.

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Boris, Draznin, and Eckel Robert H, eds. Diabetes and atherosclerosis: Molecular basis and clinical aspects. New York: Elsevier, 1993.

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International Dresden Lipid Symposium (9th 1997 Dresden, Germany). Advances in lipoprotein and atherosclerosis researh, diagnostic and treatment: Proceedings of the 9th International Dresden Lipid Symposium, held at Dresden, June 27-29, 1997. Edited by Hanefeld Markolf. Jena: G. Fischer, 1998.

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Book chapters on the topic "Atherosclerosis – Pathogenesis"

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Shah, Prediman K. "Pathogenesis of Atherosclerosis." In Essential Cardiology, 377–86. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6705-2_21.

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Gallo, Richard, and Valentin Fuster. "Pathogenesis of Atherosclerosis." In Developments in Cardiovascular Medicine, 19–46. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4375-2_2.

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Fernandez-Ortiz, Antonio, Juan J. Badimon, and Valentin Fuster. "Pathogenesis of Atherosclerosis." In Contemporary Concepts in Cardiology, 3–18. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5007-5_1.

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Cullen, P., J. Rauterberg, and S. Lorkowski. "The Pathogenesis of Atherosclerosis." In Atherosclerosis: Diet and Drugs, 3–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27661-0_1.

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Gertz, S. David, and Adi Kurgan. "Pathogenesis of Coronary Atherosclerosis." In Physiology and Pathophysiology of the Heart, 737–54. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0873-7_36.

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Haverich, Axel, and Erin Colleen Boyle. "Atherosclerosis Risk Factors." In Atherosclerosis Pathogenesis and Microvascular Dysfunction, 9–45. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-20245-3_2.

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Daria Haust, M. "Pathogenesis of Atherosclerosis: — Current Status." In Expanding Horizons in Atherosclerosis Research, 3–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71753-6_1.

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Steinberg, Daniel. "Lipoproteins and Pathogenesis of Atherosclerosis." In Pathobiology of the Human Atherosclerotic Plaque, 497–512. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3326-8_32.

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Siracuse, Jeffrey J., and Elliot L. Chaikof. "The Pathogenesis of Diabetic Atherosclerosis." In Diabetes and Peripheral Vascular Disease, 13–26. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-158-5_2.

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Fellström, Bengt, Ulla Backman, Levent Akyürek, Erik Larsson, and Lilja Zezina. "Transplantation atherosclerosis: Definition and pathogenesis." In Late Graft Loss, 39–48. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5434-5_5.

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Conference papers on the topic "Atherosclerosis – Pathogenesis"

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Gel'dyev, A. A., S. A. Pleskanovskaya, A. H. Tachmuhammedova, and O. V. Annaeva. "The value of perivascular adipose tissue in the experimental pathogenesis atherosclerosis." In Scientific achievements of the third millennium. LJournal, 2020. http://dx.doi.org/10.18411/scienceconf-05-2020-06.

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Liu, Biyue, and Dalin Tang. "Computer Simulations of the Blood Flows and the Growth of Stenosis in Arteries With Bends and Bifurcations." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203654.

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Heart attack and stroke are the chief and the 3rd largest causes of death in the United States, respectively. A heart attack occurs when the blood supply to an area of heart muscle is blocked, usually by a clot in a coronary artery; a stroke occurs when the blood supply to a region of the brain is lost. The most frequent cause of loss of blood supply to brain tissue or to heart muscle is atherosclerosis, which involves complex interactions between the artery wall and the blood flow. Caro et al first suggested that the distribution of fatty streaking in human aorta may be coincident with regions in which the shear rate at the arterial wall is locally reduced [1]. After that, intensive research has been conducted to statistically study the role of shear stress in atherosclerosis and to quantitatively determine the correlation between the low shear stress and the development of atherosclerotic plaques [2–8]. It is widely believed that fluid shear stress acting on the artery wall plays an important role in the pathogenesis of atherosclerosis. The objectives of this project are to investigate how the geometrical adaptation of atherosclerotic plaques is related to the wall shear stress (WSS) and to study the influences of the flow parameters on the growth of the atherosclerotic plaque using computational models.
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Steucke, Kerianne E., Paige A. Voigt, Eric S. Hald, and Patrick W. Alford. "Variable Modulus Muscular Thin Films for Measuring the Effect of Mechanical Environment on Vascular Contractility." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14283.

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Recent results have demonstrated that cell function is affected by local mechanical environment [1]. In vascular smooth muscle cells (VSMCs), for example, substrate stiffness can control phenotype expression and migration rate [2]. Pathologies, such as atherosclerosis, and therapeutic interventions, such as stents, can alter VSMCs’ mechanical environment. The primary function of VSMCs is vascular tone modulation via contraction and relaxation and loss of VSMCs’ contractile function may play a role in the pathogenesis of atherosclerotic plaques and restenosis of stents. To date, it is not known whether perturbation of the mechanical environment directly affects contractile function in these diseased vessels.
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"Comparison of Inflammatory Mechanisms and Model Replication Methods in the Pathogenesis of Atherosclerosis." In 2020 2nd International Symposium on the Frontiers of Biotechnology and Bioengineering (FBB 2020). Clausius Scientific Press, 2020. http://dx.doi.org/10.23977/fbb2020.031.

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Kocsy, Klaudia, Sheila Francis, Endre Kiss-Toth, Robert Lonsdale, Arshad Majid, and Jessica Redgrave. "BS22 Double positive (CD86+ MRC1+) inflammatory macrophages in the pathogenesis of carotid atherosclerosis." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.185.

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Morrison, Tina M., Gilwoo Choi, Polina A. Segalova, Christopher K. Zarins, and Charles A. Taylor. "Age-Related Changes in the Biomechanical Cyclic Strain of the Human Thoracic Aorta." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192028.

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Large vessels in the vascular system undergo progressive degeneration with aging. The widely accepted theory is the aorta enlarges and stiffens with age [1] and vascular compliance decreases [2], which increases systolic pressure, decreases diastolic pressure, and greatly affects cardiovascular health and function. Quantifying the dynamics of an aging human aorta yields insight into changes in the vascular compliance and is vital in understanding pathogenesis and progression of disease, such as atherosclerosis and aneurysm formation [3], along with medical device implantation and design.
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Guha, Snigdha, and Kaustav Majumder. "Dietary γ-glutamyl Valine in Reducing Inflammation in Endothelial Cells and in a Mouse Model for Atherosclerosis." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/mree8379.

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Cardiovascular diseases (CVDs) are the leading cause of mortality, and their prevalence is estimated at nearly 37% in the United States. Elevated blood glucose, elevated triglycerides, high blood pressure, and low levels of high-density lipoprotein, result in increased levels of inflammation and pathogenesis of various CVDs such as atherosclerosis and hypertension. Dietary γ-glutamyl valine (γ-EV), naturally found in dry beans, has exhibited beneficial biological activities to reduce chronic inflammation. The intervention of γ-EV was found to reduce the inflammatory responses in vascular endothelial cells via the activation of vascular calcium-sensing receptor (CaSR). Human tumor necrosis factor-ɑ (TNF-ɑ) was used to induce inflammation in human aortic endothelial cells (HAECs) pre-treated with γ-EV at 0.01mM, 0.1mM, and 1mM for 2 h. TNF-ɑ treatment significantly increased the expression of inflammatory adhesion molecules (VCAM-1, E-Selectin), chemokine (MCP-1), and cytokines (IL-6 and IL-8). However, the expression of these biomarkers was significantly downregulated by 1 mM γ-EV pretreatment. Furthermore, γ-EV was found to transport across the intestinal monolayer via the PepT1 transporter and paracellular pathways, with the apparent permeability (Papp) of 1.56×10–6 cm/s. The efficacy of γ-EV in reducing vascular inflammation was further evaluated in vivo, in an atherosclerotic mouse model, ApoE-/-. High-fat diet (HFD: 40 kcal% fat, 1.25% cholesterol) fed ApoE-/- mice significantly showed a reduction in the expression of inflammatory biomarkers such as VCAM-1, ICAM-1, LOX-1, MCP-1 and improved the pathological characteristics of the atherosclerotic plaques in the aorta with the γ-EV intervention (150 mg/kg BW) as compared to the mice which didn’t receive γ-EV. In addition, the FoxP3+ and CD25+ splenic T-reg cells were significantly decreased in the γ-EV-treated group. Thus, the present study highlights the potential use of γ-glutamyl peptides, as a functional food ingredient for the prevention and management of CVDs.
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Vengrenyuk, Yuliya, Theodore J. Kaplan, Luis Cardoso, Gwendalyn J. Randolph, and Sheldon Weinbaum. "Biomechanical Modeling of Atherosclerotic Lesions in ApoE Deficient Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206571.

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Cardiovascular disease remains the principal killer in the western world despite major advances in treatment of its patients [1]. It is generally accepted that sudden rupture of vulnerable plaque followed by thrombus formation underlies most cases of myocardial infarction and is responsible for more than a half of 500,000 coronary heart disease deaths every year. Although histopathological analysis of postmortem specimens have provided important data on histological features of ruptured human plaques, there is an urgent need for good representative animal models of plaque rupture. Over the last decade and a half, genetically engineered mice have been widely used to study the pathogenesis and potential treatment of atherosclerotic lesions, as well as genetic, hormonal and environmental influences on development of atherosclerosis. Though many of the features of plaque development and progression that occur in human plaques are similarly observed in murine plaques, these mouse models have long been regarded as poor models to study plaque rupture because the aortic sinus lesions seldom show any signs of fibrous cap disruption. Several recent studies reported potentially unstable atherosclerotic lesions in older apoE-deficient mice in another anatomic site, the proximal part of the brachiocephalic artery (BCA) [2, 3]. The unusual stability of aortic lesions compared to the BCA lesions in ApoE knockout mice is an unexplained paradox in developing a mouse model of plaque rupture. In this paper, we use histology based finite element analysis to evaluate peak circumferential stresses in aortic and BCA lesions from high fat fed ApoE KO mice.
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Patel, Nisha S., and Alisa Morss Clyne. "A Computational Model of Fibroblast Growth Factor-2 Binding to Isolated and Intact Cell Surface Receptors: Effects of Fibroblast Growth Factor-2 Concentration, Flow and Delivery Mode." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80798.

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Fibroblast growth factor-2 (FGF2) plays an important role in both healthy vascular cell functions and pathogenesis in cancer, atherosclerosis and reduced perfusion in diabetes (1–4). FGF2 therapy and targeted drug delivery have great potential in the treatment of such diseases, but have had little clinical success. FGF2 binding kinetics to heparan sulfate proteoglycan (HSPG) and fibroblast growth factor receptors (FGFR) have been largely studied under static conditions (5), however FGF2 binding to endothelial cells occurs physiologically under fluid flow conditions. Understanding complex FGF2 binding kinetics would enable the development of new anti- and pro-angiogenic therapeutics. We developed a computational model of FGF2 binding to FGFR and HSPG with flow to investigate the effect of fluid flow and FGF2 delivery mode on FGF2 binding to isolated or combined binding sites.
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Willett, Nick J., John Oshinski, Don Giddens, Robert Guldberg, and W. Robert Taylor. "Redox Signaling in an In Vivo Murine Model of Tailored Wall Shear Stress." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206511.

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Wall Shear Stress (WSS) has been identified as an important factor in the pathogenesis of atherosclerosis. We developed a novel murine aortic coarctation model to alter the hemodynamic environment in vivo. The model utilizes the shape memory response of nitinol clips to provide a high degree of control over aortic diameter and subsequently WSS. We employed this model to test the hypothesis that acute changes in WSS in vivo induce upregulation of inflammatory proteins mediated by Reactive Oxygen Species (ROS). WSS was mapped through a computational fluid dynamic model and correlated to inflammatory marker expression. C57B16 control mice were compared to tempol treated, apocynin treated, p47phox KO, and catalase overexpressor mice in this study. The results show that the coarctation produces low mean oscillatory WSS in the region downstream of the clip. The WSS in this region correlates to a large increase in VCAM-1 expression in wild-type mice. This WSS dependent increase in protein expression is unchanged in animal models of decreased ROS. This suggests that although the redox state is important to the overall pathogenesis of the disease, individual ROS or ROS sources may not be sufficient to inhibit a WSS dependent inflammatory response. Further analysis with this model utilizing other reagent treatments, transgenic mice, and markers will allow us to analyze the functional contribution of transcription factors, ROS, and ROS sources to WSS dependent inflammatory protein expression.
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