Accumulation of oxidative stress is considered to be a causative mediator of kidney disease, and oxidative stress can affect some key regulators of kidney homeostasis and control a number of signaling pathways that are relevant to kidney disease. The p66Shc adaptor protein was discovered more than two decades ago as a pivotal regulator of oxidative stress. Given the importance of oxidative stress in kidney homeostasis, several molecular and cellular studies using a p66Shc antagonist have depicted a role for p66Shc in renal pathophysiology. The specificity of p66Shc functions may depend upon their intracellular localization and expression in the kidney. This review focuses on the biochemical functions of the p66Shc adaptor protein, as well as its potential implications in the pathophysiology of kidney disease. In addition, the concept that pharmacologic modulation of p66Shc expression and activity may serve as a novel and effective target for the treatment of kidney disease is discussed.

译文

氧化应激的积累被认为是肾脏疾病的致病介质,氧化应激可以影响肾脏稳态的一些关键调节因子,并控制许多与肾脏疾病相关的信号通路。p66Shc衔接蛋白是二十多年前发现的氧化应激的关键调节剂。鉴于氧化应激在肾脏稳态中的重要性,一些使用p66Shc拮抗剂的分子和细胞研究已经描述了p66Shc在肾脏病理生理学中的作用。p66Shc功能的特异性可能取决于其在肾脏中的细胞内定位和表达。这篇综述着重于p66Shc衔接蛋白的生化功能,以及其在肾脏疾病病理生理学中的潜在意义。此外,还讨论了p66Shc表达和活性的药理调节可能是治疗肾脏疾病的新的有效靶标的概念。

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