Heat shock (stress response) proteins and renal ischemia/reperfusion injury
Heat shock (stress response) proteins and renal ischemia/reperfusion injury
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DOI：
10.1159/000086054
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
Kelly, KJ
中科院分区：
文献类型：
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作者：
Kelly, KJ
急性肾衰竭频繁发生，而且可能不断增加，死亡率高得令人难以接受，但目前尚无特效治疗方法。应激反应（热休克）蛋白（HSP）的诱导是一种高度保守的反应，可以保护许多细胞类型免受不同的生理和环境应激源的影响。不同大小的 HSP 家族充当分子伴侣，促进酶和其他蛋白质折叠成功能构象。损伤后，热休克蛋白被认为通过协助变性蛋白质的重新折叠和不可修复的受损蛋白质和有毒代谢物的降解、限制受损肽的聚集以及帮助新合成的必需多肽的适当折叠来促进正常功能的恢复。 HSP 还可以调节细胞凋亡和免疫功能。我们已经证明了对缺血前 6 小时而非 48 小时的热应激实验性缺血性肾损伤的功能缺陷和组织学证据的保护。热休克蛋白诱导的限制（无论是短时间的热疗还是药物）削弱了观察到的保护作用。其他研究人员已经证明了小鼠 HSP25 水平与肾缺血预处理之间的相关性。几种药物已被证明可以增加 HSP 的表达。增强这些内源性保护机制对人类疾病具有潜在益处。版权所有 (c) 2005 S. Karger AG，巴塞尔。
Acute renal failure occurs frequently, may be increasing, carries an unacceptably high mortality, yet there is no specific treatment. The induction of stress response (heat shock) proteins (HSPs) is a highly conserved response that protects many cell types from diverse physiological and environmental stressors. HSP families of different sizes function as molecular chaperones that facilitate the folding of enzymes and other proteins into functional conformations. After injury, HSPs are believed to facilitate the restoration of normal function by assisting in the refolding of denatured proteins and degradation of irreparably damaged proteins and toxic metabolites, limitation of aggregation of damaged peptides and aiding appropriate folding of newly synthesized essential polypeptides. HSPs may also regulate apoptosis and immune functions. We have demonstrated protection from the functional deficits and histological evidence of experimental ischemic renal injury with heat stress 6 but not 48 h prior to ischemia. Limitation of the induction of HSPs (either with a short period of hyperthermia or pharmacologically) attenuated the protection observed. Other investigators have demonstrated a correlation between the levels of HSP25 and renal ischemic preconditioning in the mouse. Several pharmacological agents have been shown to increase HSP expression. Enhancement of these endogenous protective mechanisms has potential benefit in human disease.Copyright (c) 2005 S. Karger AG, Basel.