Chronic intermittent hypoxia exposure-induced atherosclerosis: a brief review
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Chronic intermittent hypoxia exposure-induced atherosclerosis: a brief review Dongmei Song1 • Guoqiang Fang1 • Harly Greenberg1 • Shu Fang Liu1
Shu Fang Liu Ó Springer Science+Business Media New York 2015
Abstract Obstructive sleep apnea (OSA) is highly prevalent in the USA and is recognized as an independent risk factor for atherosclerotic cardiovascular disease. Identification of atherosclerosis risk factor attributable to OSA may provide opportunity to develop preventive measures for cardiovascular risk reduction. Chronic intermittent hypoxia (CIH) is a prominent feature of OSA pathophysiology and may be a major mechanism linking OSA to arteriosclerosis. Animal studies demonstrated that CIH exposure facilitated high-cholesterol diet (HCD)-induced atherosclerosis, accelerated the progression of existing atherosclerosis, and induced atherosclerotic lesions in the absence of other atherosclerosis risk factors, demonstrating that CIH is an independent causal factor of atherosclerosis. Comparative studies revealed major differences between CIH-induced and the classic HCD-induced atherosclerosis. Systemically, CIH was a much weaker inducer of atherosclerosis. CIH and HCD differentially activated inflammatory pathways. Histologically, CIH-induced atherosclerotic plaques had no clear necrotic core, contained a large number of CD31? endothelial cells, and had mainly elastin deposition, whereas HCD-induced plaques had typical necrotic cores and fibrous caps, contained few endothelial cells, and had mainly collagen deposition. Metabolically, CIH caused mild, but HCD caused more severe dyslipidemia. Mechanistically, CIH did not, but HCD did, cause macrophage foam cell formation. NF-jB p50 gene deletion augmented CIHinduced, but not HCD-induced atherosclerosis. These differences reflect the intrinsic differences between the two types of atherosclerosis in terms of pathological nature and underlying mechanisms and support the notion that CIH-induced atherosclerosis is a new paradigm that differs from the classic HCD-induced atherosclerosis. Keywords
Chronic intermittent hypoxia Atherosclerosis Obstructive sleep apnea Dyslipidemia Inflammation
Introduction Atherosclerotic cardiovascular disease is the leading cause of death worldwide [1, 2]. Atherosclerosis is a pathological condition underlying coronary heart disease (CHD), cerebrovascular disease and stroke, and is characterized by
& Shu Fang Liu [email protected] 1
Centers for Heart and Lung Research, and Pulmonary, Critical Care and Sleep Medicine, The Feinstein Institute for Medical Research, Hofstra North Shore-LIJ School of Medicine, 350 Community Drive, Manhasset, NY 11030, USA
accumulation of lipids, inflammatory cells, cellular debris, and vascular smooth muscle cells in the innermost layer of arterial walls [3, 4]. The mechanisms of atherosclerosis are complex and multiple, including systemic and vascular wall inflammation [3–5], dyslipidemia [6, 7], macrophage foam cell formation [5, 8], activation of immune pa
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