Heat shock protein 27 on apoptosis and the protective effect of elderly heart failure.docVIP
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Heat shock protein 27 on apoptosis and the protective effect of elderly heart failure
PAGE \* MERGEFORMAT 17
Heat shock protein 27 on apoptosis and the protective effect of elderly heart failure
[Keywords:] heat shock protein 27; aging; heart failure; apoptosis
Heat shock protein, also known as stress proteins, is a molecular chaperone, except in cell growth, development, gene transcription, protein synthesis, folding, aggregation and other aspects of the cytoskeleton play an important physiological role in addition. The cell through a variety of ways damage produced by different endogenous protection [1]. According to molecular size and degree of homology can be divided into HSPll0, HSP90, HSF70, HSP60, HSP40, small heat shock protein (Sall heat shock proteins, d-laps), HSP10 and ubiquitin and other types. heat shock protein 27 (heat shock protein 27, HSP27), also known as heat shock protein B1 (heat shock protein BHSPB1), heat shock protein 25 (heat shock protein 25 (HSP25), is a heat shock protein family The small heat shock protein subfamily (sHSP subfamilies) is an important one. HSP27 and apoptosis in recent years, the relationship between heart failure and compelling, this paper HSP27 on apoptosis and protective effect of older heart failure reviewed .
1 HSP27 anti-apoptotic mechanism
(1) HSP27 and the intracellular redox level: is the most important anti-apoptotic HSP27 and with aging is closely related to the mechanism. Reactive oxygen species (reactive oxygen species, ROS) or by exogenous oxidants generated in aerobic metabolism of intracellular , with high biological activity of oxygen free radicals can directly damage or peroxidation chain reaction through a series of widespread structural damage of biological macromolecules, and may directly alter the stability of the intracellular environment. in certain conditions, such as ischemia, hypoxia, ionizing radiation, ultraviolet radiation, chemotherapy drugs, chemical reagents can be mediated through the generation of reactive oxygen species which lead to cell apoptosis. At
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