The role of Fas in the progression of ischemic heart failure: prohypertrophy or proapoptosis

Abstract

During myocardial ischemia, cardiomyocytes can undergo apoptosis or compensatory hypertrophy. Fas expression is upregulated in the myocardial ischemia and is coupled to both apoptosis and hypertrophy of cardiomyocytes. The role of Fas in apoptosis induction or cardiomyocyte hypertrophy during ischemic conditions is, however, still unclear. Some reports suggested that Fas might induce myocardial hypertrophy. Apoptosis of ischemic cardiomyocytes and Fas expression in the nonischemic cardiomyocytes occurs during the early stage of ischemic heart failure. Hypertrophic cardiomyocytes easily undergo apoptosis in response to ischemia, after which apoptotic cardiomyocytes are replaced by fibrous tissue. In the late stage of ischemic heart failure, hypertrophy, apoptosis, and fibrosis are thought to accelerate each other and might thus form a vicious circle that eventually results in heart failure. In this review, we summarize recent advances in the understanding of the role of Fas in remodeling ischemic myocardial tissues.