Role of reactive oxygen species in the renal fibrosis  被引量:7

Role of reactive oxygen species in the renal fibrosis

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作  者:NIE Jing HOU Fan-fan 

机构地区:[1]aDivision of Nephrology, Nanfang Hospital, Southern MedicalUniversity, Research Institute of Nephrology of GuangdongProvince, Key Laboratory for Organ Failure Research, Ministry ofEducation, Guangzhou, Guangdong 510515, China

出  处:《Chinese Medical Journal》2012年第14期2598-2601,共4页中华医学杂志(英文版)

基  金:This study was supported by a grant from the National Natural Science Foundation of China (No. 30830056 and No. U0932002). Conflict of interests: None.

摘  要:Renal fibrosis is a common pathway of progressive renal diseases leading to end-stage renal disease regardless of the etiology. Accumulating evidence indicates that oxidative stress, resulting in generation of reactive oxygen species (ROS), plays a critical role in the initiation and progression of fibrotic diseases. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is the predominant enzyme source for ROS generation and is now recognized as a key mediator of cell proliferation and matrix accumulation in renal disease. Multiple stimuli and agonists, such as transforming growth factor , tumor necrosis factor, platelet derived growth factor, angiotensin II, hyperglycemia, oxidized low-density lipoprotein and albumin have been shown to alter the activity or expression of the NADPH oxidase and ultimately increase ROS production. ROS directly incites damage to biologically important macromolecules and leads to generation of the so-called advanced oxidation protein products (AOPPs) and advanced glycation end products, which are not only markers of oxidative stress but also cause renal injury. Targeting NADPH oxidase and/or reducing AOPPs production miaht be a novel strateav for the theraoeutic intervention of varietv of fibrotic kidney disorders.Renal fibrosis is a common pathway of progressive renal diseases leading to end-stage renal disease regardless of the etiology. Accumulating evidence indicates that oxidative stress, resulting in generation of reactive oxygen species (ROS), plays a critical role in the initiation and progression of fibrotic diseases. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is the predominant enzyme source for ROS generation and is now recognized as a key mediator of cell proliferation and matrix accumulation in renal disease. Multiple stimuli and agonists, such as transforming growth factor , tumor necrosis factor, platelet derived growth factor, angiotensin II, hyperglycemia, oxidized low-density lipoprotein and albumin have been shown to alter the activity or expression of the NADPH oxidase and ultimately increase ROS production. ROS directly incites damage to biologically important macromolecules and leads to generation of the so-called advanced oxidation protein products (AOPPs) and advanced glycation end products, which are not only markers of oxidative stress but also cause renal injury. Targeting NADPH oxidase and/or reducing AOPPs production miaht be a novel strateav for the theraoeutic intervention of varietv of fibrotic kidney disorders.

关 键 词:reactive oxygen species nicotinamide adenine dinucleotide phosphate oxidase renal fibrosis advanced oxidation protein products 

分 类 号:R692.9[医药卫生—泌尿科学]

 

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