Growth factor signaling for cardioprotection against oxidative stress-induced apoptosis.
The heart is subjected to oxidative stress during various clinical situations, such as ischemia-reperfusion injury and anthracycline chemotherapy. The loss of cardiac myocytes is the major problem in heart failure; thus, it is important to protect cardiac myocytes against cell death. Various growth factors, including insulin like growth factor, hepatocyte growth factor, endothelin-1, fibroblast growth factor, and transforming growth factor, have been shown to protect the heart against oxidative stress. The mechanism of growth factor-mediated cardioprotection may involve the attenuation of cardiac myocyte apoptosis. The present article summarizes the current knowledge on the molecular mechanisms of growth factor-mediated antiapoptotic signaling in cardiac myocytes. Insulin-like growth factor-1 activates phosphatidylinositol 3' -kinase and extracellular signal-regulated kinase pathways. Recent data showed that GATA-4 might be an important mediator of cardiac myocyte survival by endothelin-1 and hepatocyte growth factor. These growth factors, as well as mediators of growth factor-signaling, may be useful in therapeutic strategies against oxidative stress-induced cardiac injury.
Suzuki
Yuichiro J
YJ
Jean Mayer USDA Human Nutrition Research Center on Aging, Department of Medicine, Tufts University, Boston, MA, USA. yuichiro.suzuki@tufts.edu
D000818:Animals; D017209:Apoptosis; D006133:Growth Substances / Q000378:metabolism*; D006801:Humans; D000860:Hypoxia; D008954:Models, Biological; D032383:Myocytes, Cardiac / Q000473:pathology; D018384:Oxidative Stress; D015398:Signal Transduction
D006133:Growth Substances