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热休克蛋白70与动脉粥样硬化——保护者还是激活者?

HSP 70 and atherosclerosis--protector or activator?

作者信息

Bielecka-Dabrowa Agata, Barylski Marcin, Mikhailidis Dimitri P, Rysz Jacek, Banach Maciej

机构信息

Department of Molecular Cardionephrology and Hypertension, Medical University of Lodz, Lodz, Poland.

出版信息

Expert Opin Ther Targets. 2009 Mar;13(3):307-17. doi: 10.1517/14728220902725149.

DOI:10.1517/14728220902725149
PMID:19236153
Abstract

BACKGROUND

Atherosclerosis and its complications represent the leading cause of morbidity and mortality. Heat shock protein 70 (HSP70) protects cellular elements from injury by reducing oxidation, inflammation and apoptosis and by refolding damaged proteins. HSP70 improves viability of stressed vascular smooth muscle cells, possibly via its chaperone functions. It has been proposed that the response mounted against bacterial HSPs results in an autoimmune reaction, which has the potential to cause complement-mediated endothelial injury, and hence accelerate atherogenesis.

OBJECTIVE

to examine the roles of HSPs in atherosclerosis.

METHODS

A literature review.

RESULTS/CONCLUSIONS: The role of HSPs in atherosclerosis is controversial. HSP60 probably acts as an autoantigen, and may trigger both cell- and antibody-mediated immune responses, while HSP70 is likely to be involved in cytoprotection. The significance of this inverse relation between HSP70 and atherosclerosis has not yet been elucidated. Whether HSPs will become therapeutic targets remains to be established.

摘要

背景

动脉粥样硬化及其并发症是发病和死亡的主要原因。热休克蛋白70(HSP70)通过减少氧化、炎症和细胞凋亡以及重新折叠受损蛋白质来保护细胞成分免受损伤。HSP70可能通过其伴侣功能提高应激血管平滑肌细胞的活力。有人提出,针对细菌热休克蛋白的反应会导致自身免疫反应,这有可能引起补体介导的内皮损伤,从而加速动脉粥样硬化的发生。

目的

研究热休克蛋白在动脉粥样硬化中的作用。

方法

文献综述。

结果/结论:热休克蛋白在动脉粥样硬化中的作用存在争议。HSP60可能作为自身抗原,可能触发细胞介导和抗体介导的免疫反应,而HSP70可能参与细胞保护。HSP70与动脉粥样硬化之间这种相反关系的意义尚未阐明。热休克蛋白是否会成为治疗靶点还有待确定。

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