Oxidative Stress-Induced Signal Transduction Pathways in Cardiac Myocytes: Involvement of ROS in Heart Diseases
- 1 December 2003
- journal article
- review article
- Published by Mary Ann Liebert Inc in Antioxidants and Redox Signaling
- Vol. 5 (6), 789-794
- https://doi.org/10.1089/152308603770380098
Abstract
Reactive oxygen species (ROS) are proposed to contribute to the deterioration of cardiac function in patients with heart diseases. It has been reported that ROS are increased in the failing heart and involved in atherosclerosis, myocardial ischemia/reperfusion injury, and heart failure. Antioxidant enzymes are decreased in the decompensated heart, depressing defense mechanisms against oxidative stress. A variety of proteins, including receptors, ionic channels, transporters, and components of signal transduction pathways, are substrates of oxidation by ROS. ROS also function as signal transduction intermediates to induce transcription factor activation, gene expression, cell growth, and apoptosis. Recently, the upstream and downstream molecules of ROS in signal transduction pathways have been the subjects of intense investigation. These molecules include the mitogen-activated protein kinase family, the Rho family of small GTP binding proteins, the Src family of tyrosine kinases, Ras, and cytokines. The modulation of oxidative stress-induced signaling pathways is effective for preventing the progression of heart diseases.Keywords
This publication has 49 references indexed in Scilit:
- Oxidative stress and neutrophil activation—the two keystones of ischemia/reperfusion injuryInternational Journal of Cardiology, 2002
- Cellular response to oxidative stress: Signaling for suicide and survival*Journal of Cellular Physiology, 2002
- Integrins Play a Critical Role in Mechanical Stress–Induced p38 MAPK ActivationHypertension, 2002
- Reactive Oxygen Species in Mechanical Stress-Induced Cardiac HypertrophyBiochemical and Biophysical Research Communications, 2001
- Regulation of Mitogen-Activated Protein Kinases in Cardiac Myocytes through the Small G Protein Rac1Molecular and Cellular Biology, 2001
- Protection from reoxygenation injury by inhibition of rac1.JCI Insight, 1998
- Protein Kinase C, but Not Tyrosine Kinases or Ras, Plays a Critical Role in Angiotensin II-induced Activation of Raf-1 Kinase and Extracellular Signal-regulated Protein Kinases in Cardiac MyocytesPublished by Elsevier BV ,1996
- Mechanical stress activates protein kinase cascade of phosphorylation in neonatal rat cardiac myocytes.JCI Insight, 1995
- Small GTP-Binding Proteins and the Regulation of the Actin CytoskeletonAnnual Review of Cell Biology, 1994
- Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitroCell, 1993