横纹肌溶解肾衰的发病机制:肌红蛋白的作用。

S Holt, K Moore
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引用次数: 179

摘要

横纹肌溶解引起肾功能障碍,并伴有肾血管收缩、小管毒性和管腔梗阻。越来越多的证据表明,脂质过氧化引起的肾损伤在肾衰竭的发病机制中起重要作用。本文探讨了游离铁在这一过程中所起的中心作用。目前的数据表明,肌红蛋白的血红素中心可以启动脂质过氧化和肾损伤,而不触发游离铁的释放,这一过程是由于血红素基团从亚铁氧化态到铁氧化态和铁酰氧化态的氧化还原循环。碱性条件通过稳定反应性铁基肌红蛋白复合物来防止肌红蛋白诱导的脂质过氧化。这篇综述探讨了这些机制的证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathogenesis of renal failure in rhabdomyolysis: the role of myoglobin.

Rhabdomyolysis causes renal dysfunction associated with renal vasoconstriction, tubular toxicity and luminal obstruction. There is now accumulating evidence that renal injury, caused by lipid peroxidation, is important in the pathogenesis of renal failure. The proposed central role of free iron in this process is examined. Current data have shown that the heme center of myoglobin can initiate lipid peroxidation and renal injury without invoking release of free iron, and this process is due to redox cycling of the heme group from ferrous to ferric and to ferryl oxidation states. Alkaline conditions prevent myoglobin-induced lipid peroxidation by stabilizing the reactive ferryl myoglobin complex. This review explores the evidence for each of these mechanisms.

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