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dc.contributor.author배윤수*
dc.date.accessioned2022-11-03T16:30:59Z-
dc.date.available2022-11-03T16:30:59Z-
dc.date.issued2022*
dc.identifier.issn2211-9132*
dc.identifier.otherOAK-32507*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/262844-
dc.description.abstractOxidative stress can cause generation of uncontrolled reactive oxygen species (ROS) and lead to cytotoxic damage to cells and tissues. Recently, it has been shown that transient ROS generation can serve as a secondary messenger in receptor-mediated cell signaling. Although excessive levels of ROS are harmful, moderated levels of ROS are essential for normal physiological function. Therefore, regulating cellular ROS levels should be an important concept for development of novel therapeutics for treating diseases. The overexpression and hyperactivation of NADPH oxidase (Nox) can induce high levels of ROS, which are strongly associated with diabetic nephropathy. This review discusses the theoretical basis for development of the Nox inhibitor as a regulator of ROS homeostasis to provide emerging therapeutic opportunities for diabetic nephropathy. © 2022 by The Korean Society of Nephrology.*
dc.languageEnglish*
dc.publisherThe Korean Society of Nephrology*
dc.subjectDiabetic nephropathies*
dc.subjectNADPH oxidases*
dc.subjectNox inhibitor*
dc.subjectOxidative stress*
dc.subjectReactive oxygen species*
dc.titleNADPH oxidase inhibitor development for diabetic nephropathy through water tank model*
dc.typeReview*
dc.relation.volume41*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.indexKCI*
dc.relation.startpageS89*
dc.relation.lastpageS98*
dc.relation.journaltitleKidney Research and Clinical Practice*
dc.identifier.doi10.23876/j.krcp.21.269*
dc.identifier.scopusid2-s2.0-85139471498*
dc.author.googleLee H.E.*
dc.author.googleShim S.*
dc.author.googleChoi Y.*
dc.author.googleBae Y.S.*
dc.contributor.scopusid배윤수(15031067200)*
dc.date.modifydate20240415133331*
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자연과학대학 > 생명과학전공 > Journal papers
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