Abstract
the acute and chronic myocardial ischemia results in oxidative stress that impairs myocardial contractility and eventually leads to heart failure. However, the underlying regulatory molecular mechanisms are not fully understood. The heat shock protein 22 (Hsp22), a small-molecular-weight protein preferentially expressed in the heart, was found to be dramatically increased in the cardiac oxidative stress conditions in both human and animal models after the acute and chronic ischemia. Overexpression of Hsp22 largely protects the heart against ischemic damage. Mechanistically, overexpression of Hsp22 attenuates hypoxia-induced oxidative phosphorylation in mitochondrial and the high rate of superoxide production. Short term gene delivery of Hsp22 reduces the infarct size caused by the ischemia/reperfusion, providing a clinical therapeutic potential. This review discusses the new progress of the studies on Hsp22 by focusing on its protective effect against the excessive cardiac oxidative stress, including its adaptive induction in myocardium upon the oxidative stress, its protective role in myocardial ischemia/reperfusion, its regulation in mitochondrial oxidative phosphorylation and the underlying molecular signaling pathways promoting cell survival. This information will increase our understanding of the molecular regulation of cardiac adaption under the oxidative stress and the potential therapeutic relevance.