高迁移率族蛋白B1在心血管疾病中的作用。
Role of HMGB1 in cardiovascular diseases.
作者信息
Li Wei, Sama Andrew E, Wang Haichao
机构信息
Department of Emergency Medicine, North Shore University Hospital, New York University School of Medicine, 350 Community Drive, Manhasset, NY 11030, USA.
出版信息
Curr Opin Pharmacol. 2006 Apr;6(2):130-5. doi: 10.1016/j.coph.2005.10.010. Epub 2006 Feb 17.
A nuclear protein, high mobility group box 1 (HMGB1), is released passively by necrotic cells, and actively by macrophages/monocytes in response to exogenous and endogenous inflammatory stimuli. After binding to the receptor for advanced glycation end products (RAGE) or toll-like receptor 4 (TLR4), HMGB1 activates vascular endothelial cells and macrophages/monocytes to express proinflammatory cytokines, chemokines and adhesion molecules. Pharmacological suppression of its activities or release is protective against lethal endotoxemia and sepsis, establishing HMGB1 as a critical mediator of lethal systemic inflammation. In light of the pathogenic role of inflammation in cardiovascular diseases, we propose that HMGB1, a proinflammatory cytokine derived from both injured endothelium and activated macrophages/monocytes, could contribute to the progression of atherosclerosis and other cardiovascular diseases.
一种核蛋白，即高迁移率族蛋白B1（HMGB1），可由坏死细胞被动释放，也可由巨噬细胞/单核细胞在受到外源性和内源性炎症刺激时主动释放。与晚期糖基化终产物受体（RAGE）或Toll样受体4（TLR4）结合后，HMGB1可激活血管内皮细胞以及巨噬细胞/单核细胞，使其表达促炎细胞因子、趋化因子和黏附分子。对其活性或释放进行药理抑制可预防致死性内毒素血症和脓毒症，这表明HMGB1是致死性全身炎症的关键介质。鉴于炎症在心血管疾病中的致病作用，我们提出，HMGB1这种源自受损内皮细胞和活化巨噬细胞/单核细胞的促炎细胞因子，可能会促进动脉粥样硬化及其他心血管疾病的发展。
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