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Ralph H. Johnson Veterans Affairs Medical Center, Division of Endocrinology, Charleston, South Carolina 29401, USA
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Introduction Early epidemiological studies showed an association between infection with gram-negative bacteria and atherosclerosis ( Mendall et al . 1995 ), suggesting that toll-like receptor 4 (TLR4), a receptor for lipopolysaccharide (LPS) from
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Introduction Cardiovascular disease represents a major source of mortality in the Western world. Atherosclerosis, i.e., narrowing of the arteries as a result of lipid deposition, is the primary underlying biological cause of cardiovascular disease
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Unit of Clinical Pharmacology, Turku University Hospital, Turku, Finland
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Introduction The most acute complications of cardiovascular diseases originate from atherosclerosis, a chronic inflammatory disease of the middle- and large-sized arteries. One important risk factor for atherosclerosis is the metabolic
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Introduction Peripheral vascular disease (PVD), one of the major clinical manifestations of atherosclerosis, is highly prevalent in diabetic patients, and may cause intermittent claudication and critical limb ischemia ( Bosevski 2012 , Delbin
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higher risk for atherosclerotic cardiovascular disease in humans, we determined – in a preclinical setting – whether the chronic presence of cholestatic liver disease also induces a concomitant negative impact on atherosclerosis susceptibility
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shown to play a role in the progression of atherosclerosis ( Ohman et al . 2011 ) and were associated with coronary atherosclerotic plaque formation in humans ( Konishi et al . 2010 a , b ). Therefore, both visceral and perivascular AT accumulation and
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Department of Immunology, Monash University, Melbourne, Australia
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Department of Immunology, Monash University, Melbourne, Australia
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Introduction Coronary artery disease (CAD) has been the leading cause of death worldwide for the last few decades except in the very low-income group population ( World Health Organisation 2017 ). Atherothrombosis and atherosclerosis are the
Department of Internal Medicine, Department of Cardiology, Molecular Internal Medicine, University of New Mexico Health Sciences Center, 915 Camino de Salud NE, Albuquerque, New Mexico 87131, USA
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smooth muscle by activating thromboxane-prostanoid (TP) receptors ( Feletou & Vanhoutte 2006 ). In fact, intracoronary infusion of acetylcholine induces vasoconstriction in patients with mild and advanced atherosclerosis independent of sex ( Horio et al
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atherosclerosis and cardiovascular disease (CVD). Here, we will review the current knowledge of FABP4 in HF and CVD as well as the molecular basis by which this protein participates in the regulation of cardiac function. Obesity as a risk factor for heart
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Inflammation plays a central pathogenic role in the initiation and progression of coronary atheroma and its clinical consequences. Cytokines are the mediators of cellular inflammation and promote local inflammation in the arterial wall, which may lead to vascular smooth muscle apoptosis, degradation of the fibrin cap and plaque rupture. Platelet adhesion and thrombus formation then occur, resulting clinically in unstable angina or myocardial infarction. Recent studies have suggested that cytokines are pathogenic, contributing directly to the disease process. 'Anti-cytokine' therapy may, therefore, be of benefit in preventing or slowing the progression of cardiovascular disease. Both oestrogens and testosterone have been shown to have immune-modulating effects; testosterone in particular appears to suppress activation of pro-inflammatory cytokines. Men with low testosterone levels are at increased risk of coronary artery disease. An anti-inflammatory effect of normal physiological levels of sex hormones may, therefore, be important in atheroprotection. In this Article, we discuss some of the mechanisms involved in atherosclerotic coronary artery disease and the putative link between testosterone deficiency and atheroma formation. We present the hypothesis that the immune-modulating properties of testosterone may be important in inhibiting atheroma formation and progression to acute coronary syndrome.
