肾功能与高血压的氧化还原调控
Redox control of renal function and hypertension.
作者信息
Nistala Ravi, Whaley-Connell Adam, Sowers James R
机构信息
University of Missouri-Columbia School of Medicine, Department of Internal Medicine, Columbia, Missouri 65212, USA.
出版信息
Antioxid Redox Signal. 2008 Dec;10(12):2047-89. doi: 10.1089/ars.2008.2034.
Abstract
Loss of redox homeostasis and formation of excessive free radicals play an important role in the pathogenesis of kidney disease and hypertension. Free radicals such as reactive oxygen species (ROS) are necessary in physiologic processes. However, loss of redox homeostasis contributes to proinflammatory and profibrotic pathways in the kidney, which in turn lead to reduced vascular compliance and proteinuria. The kidney is susceptible to the influence of various extracellular and intracellular cues, including the renin-angiotensin-aldosterone system (RAAS), hyperglycemia, lipid peroxidation, inflammatory cytokines, and growth factors. Redox control of kidney function is a dynamic process with reversible pro- and anti-free radical processes. The imbalance of redox homeostasis within the kidney is integral in hypertension and the progression of kidney disease. An emerging paradigm exists for renal redox contribution to hypertension.
摘要
氧化还原稳态的丧失和过量自由基的形成在肾脏疾病和高血压的发病机制中起重要作用。诸如活性氧（ROS）等自由基在生理过程中是必需的。然而，氧化还原稳态的丧失会导致肾脏中的促炎和促纤维化途径，进而导致血管顺应性降低和蛋白尿。肾脏易受各种细胞外和细胞内信号的影响，包括肾素-血管紧张素-醛固酮系统（RAAS）、高血糖、脂质过氧化、炎性细胞因子和生长因子。肾脏功能的氧化还原控制是一个具有可逆的促自由基和抗自由基过程的动态过程。肾脏内氧化还原稳态的失衡是高血压和肾脏疾病进展的一个组成部分。肾脏氧化还原对高血压的作用存在一个新的范例。
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