Sulfaphenazole Protects Heart Against Ischemia–Reperfusion Injury and Cardiac Dysfunction by Overexpression of iNOS, Leading to Enhancement of Nitric Oxide Bioavailability and Tissue Oxygenation-Reference-Cited by-同舟云学术

Sulfaphenazole Protects Heart Against Ischemia–Reperfusion Injury and Cardiac Dysfunction by Overexpression of iNOS, Leading to Enhancement of Nitric Oxide Bioavailability and Tissue Oxygenation

Published:2009-04 Issue:4 Volume:11 Page:725-738
ISSN:1523-0864
Container-title:Antioxidants & Redox Signaling
language:en
Short-container-title:Antioxidants & Redox Signaling

Author:

Khan Mahmood¹,Mohan Iyyapu K.¹,Kutala Vijay K.¹,Kotha Sainath R.²,Parinandi Narasimham L.²,Hamlin Robert L.³,Kuppusamy Periannan¹

Affiliation:

1. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, The Ohio State University, Columbus, Ohio.

2. Davis Heart and Lung Research Institute, Division of Pulmonary and Critical Care Medicine; Department of Internal Medicine, The Ohio State University, Columbus, Ohio.

3. Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio.

Publisher

Mary Ann Liebert Inc

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry,Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry

Link

http://www.liebertpub.com/doi/pdf/10.1089/ars.2008.2155

Reference69 articles.

1. Nitric oxide synthases: structure, function and inhibition

2. The relationship between oxygen radical generation and impairment of myocardial energy metabolism following post-ischemic reperfusion,

3. Atorvastatin-induced cardioprotection is mediated by increasing inducible nitric oxide synthase and consequent S-nitrosylation of cyclooxygenase-2

4. STRESS signaling pathways that modulate cardiac myocyte apoptosis

5. Inhibition of HtrA2/Omi ameliorates heart dysfunction following ischemia/reperfusion injury in rat heart in vivo

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