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NADPH 氧化酶作为治疗草酸诱导肾脏损伤的靶点。

NADPH oxidase as a therapeutic target for oxalate induced injury in kidneys.

机构信息

Department of Pathology, Immunology & Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL 32610, USA.

出版信息

Oxid Med Cell Longev. 2013;2013:462361. doi: 10.1155/2013/462361. Epub 2013 Jun 6.

DOI:10.1155/2013/462361
PMID:23840917
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3690252/
Abstract

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.

摘要

烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶家族的主要作用是催化超氧化物和其他活性氧(ROS)的产生。这些 ROS 反过来作为细胞信号转导和细胞周期中的信使发挥关键作用,但当它们过量产生时,会导致氧化应激(OS)。目前,肾脏中的氧化应激被认为是肾脏损伤和炎症的主要原因,导致各种病理紊乱。在这篇综述中,我们讨论了草酸盐通过在肾脏不同细胞位置表达的 NADPH 氧化酶同工型产生活性氧,从而产生氧化应激的可能作用。大多数肾细胞都会产生 ROS,最近的数据表明,NADPH 氧化酶、ROS 和炎症的上调基因表达之间存在直接相关性。肾脏组织中多种 NADPH 氧化酶同工型的表达很可能会影响未来使用不同抗氧化剂和 NADPH 氧化酶抑制剂来最小化高草酸尿症诱导的肾结石病中的 OS 和肾脏组织损伤。

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