Ablation of Peroxiredoxin V Exacerbates Ischemia/Reperfusion-Induced Kidney Injury in Mice

被引：12

作者：

Park, Jiyoung ^{[1
]}

Lee, Eun Gyeong ^{[1
]}

Yi, Ho Jin ^{[2
]}

Kim, Nam Hee ^{[1
]}

Rhee, Sue Goo ^{[3
,4
]}

Woo, Hyun Ae ^{[1
,2
]}

机构：

[1] Ewha Womans Univ, Coll Pharm, Grad Sch Pharmaceut Sci, Seoul 120750, South Korea

[2] Ewha Womans Univ, Coll Pharm, Grad Sch Appl Sci & Technol Skin Hlth & Aesthet, Seoul 120750, South Korea

[3] Yonsei Univ, Yonsei Biomed Res Inst, Coll Med, Seoul 120752, South Korea

[4] NHLBI, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA

来源：

ANTIOXIDANTS | 2020年 / 9卷 / 08期

基金：

新加坡国家研究基金会;

关键词：

peroxiredoxin V; reactive oxygen species; renal ischemia; reperfusion; renal dysfunction; ISCHEMIA-REPERFUSION INJURY; CYSTEINE SULFINIC ACID; OXIDATIVE STRESS; SULFIREDOXIN; PATHOPHYSIOLOGY; INACTIVATION; INHIBITION; MECHANISM; APOPTOSIS; DISEASE;

D O I：

10.3390/antiox9080769

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Ischemia/reperfusion (I/R) is one of the major causes of acute kidney injury (AKI) and associated with increased mortality and progression to chronic kidney injury (CKI). Molecular mechanisms underlying I/R injury involve the production and excessive accumulation of reactive oxygen species (ROS). Peroxiredoxin (Prx) V, a cysteine-dependent peroxidase, is located in the cytosol, mitochondria, and peroxisome and has an intensive ROS scavenging activity. Therefore, we focused on the role of Prx V during I/R-induced AKI using Prx V knockout (KO) mice. Ablation of Prx V augmented tubular damage, apoptosis, and declined renal function. Prx V deletion also showed higher susceptibility to I/R injury with increased markers for oxidative stress, ER stress, and inflammation in the kidney. Overall, these results demonstrate that Prx V protects the kidneys against I/R-induced injury.

引用

页码：1 / 12

页数：12

共 45 条

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