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Peroxisome proliferator-activated receptor-alpha is renoprotective in doxorubicin-induced glomerular injury
Zhou, Yunfeng1; Kong, Xiaomu1; Zhao, Pan1; Yang, Hang1; Chen, Lihong1; Miao, Jing2; Zhang, Xiaoyan1; Yang, Jichun1; Ding, Jie2; Guan, Youfei1,3,4
关键词doxorubicin fenofibrate peroxisome proliferator-activated receptor podocyte injury proteinuria
刊名KIDNEY INTERNATIONAL
2011-06-01
DOI10.1038/ki.2011.17
79期:12页:1302-1311
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Urology & Nephrology
研究领域[WOS]Urology & Nephrology
关键词[WOS]ACUTE-RENAL-FAILURE ; NEPHROTIC SYNDROME ; PODOCYTE INJURY ; DIABETIC-NEPHROPATHY ; METABOLIC SYNDROME ; LIPID-METABOLISM ; TUBULAR CELLS ; EXPRESSION ; PROTECTS ; MICE
英文摘要

Doxorubicin (DOX) is an anthracycline antibiotic utilized in antitumor therapy; however, its clinical use is frequently impeded by renal toxic effects. As peroxisome proliferator-activated receptor-alpha (PPAR-alpha) has renoprotective effects in drug-related kidney injuries, we tested its ability to inhibit DOX-induced renal injury. Although both male PPAR-alpha knockout mice and their wild-type littermates (pure 129/SvJ background) had significant proteinuria 4 weeks after DOX treatment, those with deletion of PPAR-alpha had more severe proteinuria. This was associated with more serious podocyte foot process effacement compared with wild-type mice. In contrast, the PPAR-alpha agonist fenofibrate effectively reduced proteinuria and attenuated DOX-induced podocyte foot process effacement. Consistently, glomerular nephrin expression was significantly lower in the knockout compared with wild-type mice following DOX treatment. Fenofibrate therapy significantly blunted the reduction in glomerular nephrin levels in DOX-treated wild-type mice. In cultured podocytes, DOX induced apoptosis, increased cleaved caspase-3 levels, and decreased Bcl-2 expression, all attenuated by pretreatment with fenofibrate. Thus, PPAR-alpha deficiency exacerbates DOX-related renal injury, in part, due to increased podocyte apoptosis. Kidney International (2011) 79, 1302-1311; doi:10.1038/ki.2011.17; published online 2 March 2011

语种英语
WOS记录号WOS:000291093300006
项目编号30890041 ; 81030003 ; 30870905 ; 30725033 ; 2010CB912503 ; NIDDK RO1 065074-04 ; PPG 038226
资助机构National Natural Science Foundation of China (NSFC) ; Ministry of Science and Technology ; National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
引用统计
被引频次:31[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/64746
专题北京大学第三临床医学院_心脏外科
北京大学基础医学院
北京大学第一临床医学院_儿科
北京大学第二临床医学院_风湿免疫科
作者单位1.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 1000191, Peoples R China
2.Peking Univ, Hosp 1, Dept Pediat, Beijing 1000191, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Ctr Diabet, Beijing 1000191, Peoples R China
4.Peking Univ, Hlth Sci Ctr, Minist Educ, Key Lab Cardiovasc Sci, Beijing 1000191, Peoples R China
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Zhou, Yunfeng,Kong, Xiaomu,Zhao, Pan,et al. Peroxisome proliferator-activated receptor-alpha is renoprotective in doxorubicin-induced glomerular injury[J]. KIDNEY INTERNATIONAL,2011,79(12):1302-1311.
APA Zhou, Yunfeng.,Kong, Xiaomu.,Zhao, Pan.,Yang, Hang.,Chen, Lihong.,...&Guan, Youfei.(2011).Peroxisome proliferator-activated receptor-alpha is renoprotective in doxorubicin-induced glomerular injury.KIDNEY INTERNATIONAL,79(12),1302-1311.
MLA Zhou, Yunfeng,et al."Peroxisome proliferator-activated receptor-alpha is renoprotective in doxorubicin-induced glomerular injury".KIDNEY INTERNATIONAL 79.12(2011):1302-1311.
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