Activation of NADPH Oxidase During Progression of Cardiac Hypertrophy to Failure
Top Cited Papers
- 1 October 2002
- journal article
- research article
- Published by Wolters Kluwer Health in Hypertension
- Vol. 40 (4) , 477-484
- https://doi.org/10.1161/01.hyp.0000032031.30374.32
Abstract
Increased reactive oxygen species (ROS) production is implicated in the pathophysiology of left ventricular (LV) hypertrophy and heart failure. However, the enzymatic sources of myocardial ROS prod...Keywords
This publication has 15 references indexed in Scilit:
- Reactive Oxygen Species Modulate Angiotensin II-Induced β-Myosin Heavy Chain Gene Expression via Ras/Raf/Extracellular Signal-Regulated Kinase Pathway in Neonatal Rat CardiomyocytesBiochemical and Biophysical Research Communications, 2001
- Expression of p22-phox and gp91-phox, Essential Components of NADPH Oxidase, Increases after Myocardial InfarctionBiochemical and Biophysical Research Communications, 2001
- Redox regulation of MAPK pathways and cardiac hypertrophy in adult rat cardiac myocytePublished by Elsevier ,2001
- Extracellular Signal-regulated Kinase Plays an Essential Role in Hypertrophic Agonists, Endothelin-1 and Phenylephrine-induced Cardiomyocyte HypertrophyJournal of Biological Chemistry, 2000
- Role of oxidative stress in cardiovascular diseasesJournal Of Hypertension, 2000
- Paracrine and autocrine effects of nitric oxide on myocardial functionPharmacology & Therapeutics, 2000
- Stress Pathways and Heart FailureCell, 1999
- Cellular and molecular mechanisms of endothelial cell dysfunction.Journal of Clinical Investigation, 1997
- NADPH-oxidase-dependent Superoxide Production by Myocyte-derived H9c2 Cells: Influence of Ischemia, Heat Shock, Cycloheximide and Cytochalasin DJournal of Molecular and Cellular Cardiology, 1997
- Differential Protein Expression and Subcellular Distribution of TGFβ1,β2andβ3in Cardiomyocytes During Pressure Overload-induced HypertrophyJournal of Molecular and Cellular Cardiology, 1997