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Role of p66shc in Renal Toxicity of Oleic Acid
Author(s) -
István Arany,
Jeb S. Clark,
Dustin K Reed,
Luis A. Juncos,
Mehul Dixit
Publication year - 2013
Publication title -
american journal of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.394
H-Index - 85
eISSN - 1421-9670
pISSN - 0250-8095
DOI - 10.1159/000354357
Subject(s) - oxidative stress , reactive oxygen species , mitochondrial ros , endocrinology , medicine , oxidative phosphorylation , chemistry , biochemistry
Adult and childhood obesity is an independent risk factor in development of chronic kidney disease (CKD) and its progression to end-stage kidney disease. Pathologic consequences of obesity include non-esterified fatty acid-induced oxidative stress and consequent injury. Since the serine36-phosphorylated p66shc is a newly recognized mediator of oxidative stress and kidney injury, we studied its role in oleic acid (OA)-induced production of reactive oxygen species (ROS), mitochondrial depolarization and injury in cultured renal proximal tubule cells.

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