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Arquivos Brasileiros de Cardiologia Feb 2001Observational studies have attributed a protective effect to alcohol consumption on the development of atherosclerosis and cardiovascular morbidity and mortality.... (Review)
Review
Observational studies have attributed a protective effect to alcohol consumption on the development of atherosclerosis and cardiovascular morbidity and mortality. Alcohol intake in the amount of one to two drinks per day results in an estimated 20-40% reduction in cardiovascular events. An additional protective effect, according to major cohort studies, has been attributed to wine, probably due to antioxidant effects and platelet antiaggregation agents. On the other hand, the influence of different patterns of alcohol consumption and environmental factors may explain a great part of the additional effect of wine. Protection may be mediated by modulation of other risk factors, because alcohol increases HDL-C, produces a biphasic response on blood pressure, and modulates the endothelial function, while it neither increases body weight nor impairs glucose-insulin homeostasis. Alcohol may also have a direct effect on atherogenesis. Despite these favorable effects, the current evidence is not enough to justify prescribing alcohol to prevent cardiovascular disease.
Topics: Alcohol Drinking; Arteriosclerosis; Coronary Disease; Humans; Risk Factors; Wine
PubMed: 11270318
DOI: 10.1590/s0066-782x2001000200009 -
Journal of Atherosclerosis and... 2003Atherosclerosis is primarily a lesion that progresses due to a series of reactions that are induced by repair of injured intima. The intercellular networking that occurs... (Review)
Review
Atherosclerosis is primarily a lesion that progresses due to a series of reactions that are induced by repair of injured intima. The intercellular networking that occurs among smooth muscle cells, macrophages, T lymphocytes and endothelial cells leads to a fibroproliferative response, in which the extracellular matrix (ECM) plays an important role. The ECM, composed of a mixture of vastly different macromolecules including collagen, elastin, glycoproteins and proteoglycans, confers tensile strength and viscoelasticity to the arterial wall. Each component of the ECM possesses unique structural properties that determine its own roles during the development of atherosclerotic plaques. Not only does the ECM provide the structural integrity of the plaques, but it also participates in several key events such as cell migration and proliferation, lipoprotein retention and thrombosis. The various matrix metalloproteinases (MMPs), major enzymes in ECM degradation, and their inhibitors (tissue inhibitors of MMPs) are demonstrated in plaque. An excess of MMPs over inhibitors contributes significantly to ECM destruction rendering the plaque more prone to rupture. Accumulating information on the molecular regulation of ECM synthesis and degradation will help investigators attain a more thorough understanding of the mechanisms of plaque formation and plaque instability and rupture.
Topics: Arteriosclerosis; Extracellular Matrix; Humans; Metalloproteases
PubMed: 14718743
DOI: 10.5551/jat.10.267 -
British Medical Journal Jul 1955
Topics: Arteriosclerosis; Endopeptidases; Hydrolases; Peptide Hydrolases
PubMed: 14378639
DOI: No ID Found -
The American Journal of Pathology Jul 2004Animal models are designed to be preliminary tools for better understanding of the pathogenesis, improvement in diagnosis, prevention, and therapy of arteriosclerosis in... (Review)
Review
Animal models are designed to be preliminary tools for better understanding of the pathogenesis, improvement in diagnosis, prevention, and therapy of arteriosclerosis in humans. Attracted by the well-defined genetic systems, a number of investigators have begun to use the mouse as an experimental system for arteriosclerosis research. Hundreds of inbred lines have been established, and the genetic map is relatively well defined, and both congenic strains and recombinant strains are available to facilitate genetic experimentation. Because arteriosclerosis is a complicated disease, which includes spontaneous (native) atherosclerosis, transplant arteriosclerosis, vein graft atherosclerosis, and angioplasty-induced restenosis, several mouse models for studying all types of arteriosclerosis have recently been established. Using these mouse models, much knowledge concerning the pathogenesis of the disease and therapeutic intervention has been gained, eg, origins of endothelial and smooth muscle cells in lesions of transplant and vein graft atherosclerosis. This review will not attempt to cover all aspects of mouse models, rather focus on models of arterial injuries, vein grafts, and transplant arteriosclerosis, by which the major progress in understanding the mechanisms of the disease has been made. This article will also point out (dis)advantages of a variety of models, and how the models can be appropriately chosen for different purposes of study.
Topics: Animals; Arteries; Arteriosclerosis; Carotid Arteries; Disease Models, Animal; Forecasting; Graft Occlusion, Vascular; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Stents
PubMed: 15215157
DOI: 10.1016/S0002-9440(10)63270-1 -
Arteriosclerosis, Thrombosis, and... Sep 2021
Topics: Animals; Anniversaries and Special Events; Arteriosclerosis; Biomedical Research; Editorial Policies; History, 20th Century; History, 21st Century; Humans; Periodicals as Topic; Thrombosis
PubMed: 34432483
DOI: 10.1161/ATVBAHA.121.316755 -
International Journal of Molecular... Jul 2021Fundamental pancreatic β-cell function is to produce and secrete insulin in response to blood glucose levels. However, when β-cells are chronically exposed to... (Review)
Review
Favorable Effects of GLP-1 Receptor Agonist against Pancreatic β-Cell Glucose Toxicity and the Development of Arteriosclerosis: "The Earlier, the Better" in Therapy with Incretin-Based Medicine.
Fundamental pancreatic β-cell function is to produce and secrete insulin in response to blood glucose levels. However, when β-cells are chronically exposed to hyperglycemia in type 2 diabetes mellitus (T2DM), insulin biosynthesis and secretion are decreased together with reduced expression of insulin transcription factors. Glucagon-like peptide-1 (GLP-1) plays a crucial role in pancreatic β-cells; GLP-1 binds to the GLP-1 receptor (GLP-1R) in the β-cell membrane and thereby enhances insulin secretion, suppresses apoptotic cell death and increase proliferation of β-cells. However, GLP-1R expression in β-cells is reduced under diabetic conditions and thus the GLP-1R activator (GLP-1RA) shows more favorable effects on β-cells at an early stage of T2DM compared to an advanced stage. On the other hand, it has been drawing much attention to the idea that GLP-1 signaling is important in arterial cells; GLP-1 increases nitric oxide, which leads to facilitation of vascular relaxation and suppression of arteriosclerosis. However, GLP-1R expression in arterial cells is also reduced under diabetic conditions and thus GLP-1RA shows more protective effects on arteriosclerosis at an early stage of T2DM. Furthermore, it has been reported recently that administration of GLP-1RA leads to the reduction of cardiovascular events in various large-scale clinical trials. Therefore, we think that it would be better to start GLP-1RA at an early stage of T2DM for the prevention of arteriosclerosis and protection of β-cells against glucose toxicity in routine medical care.
Topics: Arteriosclerosis; Diabetes Mellitus, Type 2; Glucagon-Like Peptide-1 Receptor; Humans; Hyperglycemia; Incretins; Insulin-Secreting Cells
PubMed: 34360682
DOI: 10.3390/ijms22157917 -
Journal of Internal Medicine Mar 2000This review discusses three stages in the life history of an atheroma: initiation, progression and complication. Recruitment of mononuclear leucocytes to the intima... (Review)
Review
This review discusses three stages in the life history of an atheroma: initiation, progression and complication. Recruitment of mononuclear leucocytes to the intima characterizes initiation of the atherosclerotic lesion. Specific adhesion molecules expressed on the surface of vascular endothelial cells mediate leucocyte adhesion: the selectins and members of the immunoglobulin superfamily such as vascular cell adhesion molecule-1 (VCAM-1). Once adherent, the leucocytes enter the artery wall directed by chemoattractant chemokines such as macrophage chemoattractant protein-1 (MCP-1). Modified lipoproteins contain oxidized phospholipids which can elicit expression of adhesion molecule and cytokines implicated in early atherogenesis. Progression of atheroma involves accumulation of smooth muscle cells which elaborate extracellular matrix macromolecules. These processes appear to result from an eventual net positive balance of growth stimulatory versus growth inhibitory stimuli, including proteins (cytokines and growth factors) and small molecules (e.g. prostanoids and nitric oxide). The clinically important complications of atheroma usually involve thrombosis. Arterial stenoses by themselves seldom cause acute unstable angina or acute myocardial infarction. Indeed, sizeable atheroma may remain silent for decades or produce only stable symptoms such as angina pectoris precipitated by increased demand. Recent research has furnished new insight into the molecular mechanisms that cause transition from the chronic to the acute phase of atherosclerosis. Thrombus formation usually occurs because of a physical disruption of atherosclerotic plaque. The majority of coronary thromboses result from a rupture of the plaque's protective fibrous cap, which permits contact between blood and the highly thrombogenic material located in the lesion's lipid core, e.g. tissue factor. Interstitial collagen accounts for most of the tensile strength of the plaque's fibrous cap. The amount of collagen in the lesion's fibrous cap depends upon its rate of biosynthesis stimulated by factors released from platelets (e.g. transforming growth factor beta or platelet-derived growth factor), but inhibited by gamma interferon, a product of activated T cells found in plaques. Degradation by specialized enzymes (matrix metalloproteinases) also influences the level of collagen in the plaque's fibrous cap. Such studies illustrate how the application of cellular and molecular approaches has fostered a deeper understanding of the pathogenesis of atherosclerosis. This increased knowledge of the basic mechanisms enables us to understand how current therapies for atherosclerosis may act. Moreover, the insights derived from recent scientific advances should aid the discovery of new therapeutic targets that would stimulate development of novel treatments. Such new treatments could further reduce the considerable burden of morbidity and mortality due to this modern scourge, and reduce reliance on costly technologies that address the symptoms rather than the cause of atherosclerosis.
Topics: Arteriosclerosis; Humans
PubMed: 10762452
DOI: 10.1046/j.1365-2796.2000.00654.x -
American Heart Journal Dec 1994To understand the process of atherosclerosis, the homeostatic and protective functions of the endothelium must be considered. The endothelium serves as the interface... (Review)
Review
To understand the process of atherosclerosis, the homeostatic and protective functions of the endothelium must be considered. The endothelium serves as the interface between blood flow and the vascular tissues. It normally regulates vascular tone and structure through the release of vasoactive substances and maintenance of a nonthrombogenic surface. Endothelial dysfunction, which results from biochemical and hemodynamic stresses associated with cardiovascular risk factors, causes an imbalance in the expression of vasodilating and vasoconstricting substances, as well as excess production of chemoattractant molecules and growth factors. Endothelial dysfunction in the presence of elevated cholesterol levels fosters the development of fatty streaks, which represent the early stage of atherosclerotic plaque. The unstable progression of atherosclerosis can be interrupted and even reversed in both animals and humans, although the exact clinical correlates of progression and regression are not fully understood.
Topics: Animals; Arteriosclerosis; Blood Vessels; Humans; Thrombosis
PubMed: 7977010
DOI: 10.1016/0002-8703(94)90251-8 -
Reviews in Cardiovascular Medicine Mar 2022Obstructive sleep apnea (OSA) is a common disorder worldwide. It is associated with myocardial remodeling and arteriosclerosis in patients with hypertension. Our study...
BACKGROUND
Obstructive sleep apnea (OSA) is a common disorder worldwide. It is associated with myocardial remodeling and arteriosclerosis in patients with hypertension. Our study investigated the relationship between OSA severity and arteriosclerosis and blood pressure in an Asian population.
METHODS
We enrolled 365 subjects from July 2018 to December 2020 at Ruijin Hospital. We recorded data from the medical history and collected blood samples from all participants. We performed 24-hour ambulatory Blood Pressure (BP) monitoring and Carotid-femoral pulse wave velocity (cf-PWV) measurements. Overnight polysomnography (PSG) was performed using Respironics Alice PDxSleepware.
RESULTS
PSG was performed in a total of 365 subjects; mean age of 49.1 ± 12.8 years and Body Mass Index (BMI) 28.1 ± 3.8 kg/m2. The majority (89.3%) were male. The office systolic BP was significantly higher in the moderate to severe group than mild OSA group (148 ± 21 mmHg vs 139 ± 19 mmHg, < 0.01). The subjects with moderate to severe OSA presented higher cf-PWV values than those in the mild group (10.03 ± 3.67 m/s vs 7.62 ± 1.48 m/s, < 0.01). BMI was significantly higher in the moderate to severe than the mild OSA groups (28.3 ± 4.0 kg/m2 vs 27.5 ± 3.2 kg/m2, < 0.05). The Pearson correlation showed that the apnea-hypopnea index (AHI) was significantly and positively correlated with cf-PWV ( = 0.217, < 0.01), Age ( = 0.148, 0.01), BMI ( = 0.228, < 0.01) and HbA1c ( = 0.172, < 0.01). After adjusting for age, BMI, low density lipoprotein cholesterin (LDL-c), FGB, AHI, estimated Glomerular Filtration Rate (eGFR), Night BP, office diastolic BP and Day BP in Logistic regression model, AHI (OR = 1.03, 95% CI: 1.01-1.05) and office diastolic pressure (OR = 1.04, 95% CI: 1.00-1.08) and age (OR = 1.12, 95% CI: 1.06-1.19) were independent risk factors for arteriosclerosis.
CONCLUSIONS
The severity of OSA was positively correlated with pulse wave velocity. AHI, office BP and age were independent risk factors for arteriosclerosis.
Topics: Adult; Arteriosclerosis; Blood Pressure Monitoring, Ambulatory; Female; Humans; Male; Middle Aged; Polysomnography; Pulse Wave Analysis; Sleep Apnea, Obstructive
PubMed: 35345261
DOI: 10.31083/j.rcm2303094 -
Kidney International. Supplement Jul 1999Lipid moieties may have direct or indirect effects on the kidney. The association of aortic atherosclerosis and renal artery stenosis has focused interest on this as an... (Review)
Review
BACKGROUND
Lipid moieties may have direct or indirect effects on the kidney. The association of aortic atherosclerosis and renal artery stenosis has focused interest on this as an important cause of end-stage renal failure. This article seeks to examine the evidence for the entity of atherosclerotic nephropathy.
METHODS
Published data on the incidence of atherosclerotic renal artery stenosis as the cause of end-stage renal failure are presented, as well as the associated features of atherosclerotic renal stenosis.
RESULTS
Atherosclerotic renal artery stenosis (ARAS) has been estimated to be the cause of between 14 and 25% of patients reaching end-stage renal failure in older age groups. There is considerable evidence of proteinuria in patients with ARAS. Recent data have shown that renal length may decrease by 1 cm or more in 35% of kidneys with > 60% stenosis. However, other data suggest that renal function in kidneys without renal artery stenosis but with contralateral renal artery stenosis may be similarly decreased.
CONCLUSION
Many processes contribute to renal dysfunction in atherosclerotic aortic disease. Although ischemia may play a role, there is considerable evidence that processes such as atheroembolic disease may be important, and it would be better to use the term "atherosclerotic nephropathy" for this important disease entity.
Topics: Arteriosclerosis; Humans; Kidney Diseases
PubMed: 10412750
DOI: 10.1046/j.1523-1755.1999.07126.x