Coronary artery disease (CAD) is the leading cause of death worldwide. The efficacy and safety of statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors) in primary and secondary prevention of CAD are confirmed in several large studies. It is well known that statins have some pleiotropic, anti-atherosclerotic effects. We review the molecular mechanisms underlying the beneficial effects of statins revealed in recently published studies. Endothelial cell injury is regarded as the classic stimulus for the development of atherosclerotic lesions. In addition, the inflammatory process plays an important role in the aetiology of atherosclerosis. In particular, chronic inflammation plays a key role in coronary artery plaque instability and subsequent occlusive thrombosis. Our previous reports and others have demonstrated beneficial effects of statins on endothelial dysfunction and chronic inflammation in CAD. A better understanding of the molecular mechanism underlying the effectiveness of statins against atherosclerosis may provide a novel therapeutic agent for the treatment of coronary atherosclerosis. The present review summarizes the cellular and molecular mechanism of statins against coronary atherosclerosis.
- endothelial progenitor cells
- toll-like receptor 4
Abbreviations: ACS, acute coronary syndrome; CABG, coronary artery bypass grafting; CAD, coronary artery disease; CRP, C-reactive protein; EPC, endothelial progenitor cell; HMG-CoA, 3-hydroxy-3-methylglutaryl-coenzyme A; LDL-C, low-density lipoprotein-cholesterol; IL, interleukin; LPS, lipopolysaccharide; MFI, mean fluorescent intensity; NF-κB, nuclear factor κB; PAMP, pathogen-associated molecular pattern; SIRT1, silent information regulator 1; TLR, toll-like receptor; TNF-α, tumour necrosis factor α
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