P
Paul N. Epstein
Researcher at University of Louisville
Publications - 88
Citations - 4876
Paul N. Epstein is an academic researcher from University of Louisville. The author has contributed to research in topics: Diabetic nephropathy & Oxidative stress. The author has an hindex of 38, co-authored 88 publications receiving 4449 citations.
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Journal ArticleDOI
Protection of Cardiac Mitochondria by Overexpression of MnSOD Reduces Diabetic Cardiomyopathy
TL;DR: Overexpression of MnSOD to the heart provided extensive protection to diabetic mitochondria and provided overall protection to the diabetic heart.
Journal ArticleDOI
Catalase protects cardiomyocyte function in models of type 1 and type 2 diabetes.
Gang Ye,Naira Metreveli,Rajakumar V. Donthi,Shen Xia,Ming Xu,Edward C. Carlson,Paul N. Epstein +6 more
TL;DR: Data show that both type 1 and type 2 diabetes induce damage at the level of individual myocytes, and that this damage occurs through mechanisms utilizing ROS.
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Cardiac mitochondrial damage and biogenesis in a chronic model of type 1 diabetes
Xia Shen,Shirong Zheng,Visith Thongboonkerd,Ming Xu,William M. Pierce,Jon B. Klein,Paul N. Epstein +6 more
TL;DR: Results show that mitochondria are a primary target in the diabetic heart, probably due to oxidative stress, and that this damage coincides with and may stimulate mitochondrial biogenesis.
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Diminished Autophagy Limits Cardiac Injury in Mouse Models of Type 1 Diabetes
Xianmin Xu,Satoru Kobayashi,Kai Chen,Derek Timm,Paul A. Volden,Yuan Huang,James Gulick,Zhenyu Yue,Jeffrey Robbins,Paul N. Epstein,Qiangrong Liang +10 more
TL;DR: The findings demonstrate that the diminished autophagy is an adaptive response that limits cardiac dysfunction in type 1 diabetes, presumably through up-regulation of alternative autophagic and mitophagy.
Journal ArticleDOI
Metallothionein Prevents Diabetes-Induced Deficits in Cardiomyocytes by Inhibiting Reactive Oxygen Species Production
TL;DR: The data show that diabetes induces damage at the level of individual myocyte, and diabetes increases ROS production via angiotensin II and flavoprotein enzyme-dependent pathways.