Broad Suppression of NADPH Oxidase Activity Exacerbates Ischemia/Reperfusion Injury Through Inadvertent Downregulation of Hypoxia-inducible Factor-1α and Upregulation of Peroxisome Proliferator–activated Receptor-α-Reference-Cited by-同舟云学术

Broad Suppression of NADPH Oxidase Activity Exacerbates Ischemia/Reperfusion Injury Through Inadvertent Downregulation of Hypoxia-inducible Factor-1α and Upregulation of Peroxisome Proliferator–activated Receptor-α

Published:2013-04-12 Issue:8 Volume:112 Page:1135-1149
ISSN:0009-7330
Container-title:Circulation Research
language:en
Short-container-title:Circ Res

Author:

Matsushima Shouji¹,Kuroda Junya¹,Ago Tetsuro¹,Zhai Peiyong¹,Ikeda Yoshiyuki¹,Oka Shinichi¹,Fong Guo-Hua¹,Tian Rong¹,Sadoshima Junichi¹

Affiliation:

1. From the Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, University of Medicine and Dentistry of New Jersey, Newark, NJ (S.M., J.K., T.A., P.Z., Y.I., S.O., J.S.); Center for Vascular Biology, University of Connecticut Health Center, Farmington, CT (G.-H.F.); and Mitochondria and Metabolism Center, University of Washington, Seattle, WA (R.T.).

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

Reference37 articles.

1. Impaired Long-Chain Fatty Acid Oxidation and Contractile Dysfunction in the Obese Zucker Rat Heart

2. Regulation of myocardial growth and death by NADPH oxidase

3. Upregulation of Nox4 by Hypertrophic Stimuli Promotes Apoptosis and Mitochondrial Dysfunction in Cardiac Myocytes

4. Involvement of Nox2 NADPH Oxidase in Adverse Cardiac Remodeling After Myocardial Infarction

5. NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart

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