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SIRT1: A novel target to prevent atherosclerosis
Author(s) -
Yu Wei,
Fu YuCai,
Chen ChunJuan,
Wang Xin,
Wang Wei
Publication year - 2009
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22240
Subject(s) - downregulation and upregulation , enos , pathogenesis , nitric oxide , regulator , endothelium , foam cell , apoptosis , microbiology and biotechnology , chemistry , lipoprotein , cholesterol , immunology , biology , nitric oxide synthase , endocrinology , biochemistry , gene
Atherosclerosis is a chronic immuno‐inflammatory disease associated with blood lipids disorder. Many studies have demonstrated that caloric restriction (CR) can prevent atherosclerosis and extend lifespan. Sir2 protein, mammal's SIRT1, has been reported to at least partly contribute to the protective effect of CR. Hence, we hypothesize that SIRT1 is a key regulator in the pathogenesis of atherosclerosis and that upregulation of SIRT1 in endothelial cells may mimic CR's beneficial effect on vascular health. The recent studies have demonstrated that endothelial SIRT1 is an anti‐atherosclerosis factor and the possible mechanism may be related to inhibit oxidized low‐density lipoprotein (oxLDL)‐induced apoptosis, upregulate endothelial nitric oxide synthase (eNOS) expression, and improve endothelium relaxation function. We infer that SIRT1 may be a novel target for atherosclerosis prevention and treatment. J. Cell. Biochem. 108: 10–13, 2009. © 2009 Wiley‐Liss, Inc.