Role of heat shock transcriptional factor 1 and heat shock proteins in cardiac hypertrophy.

Abstract

Cardiac hypertrophy is an independent risk factor for cardiovascular disease. Initially, cardiac hypertrophy is an adaptive response to increased wall stress, but sustained stress leads to heart failure. It remains unclear how the transition from adaptive cardiac hypertrophy to maladaptive cardiac hypertrophy occurs. It has been postulated that there are two forms of cardiac hypertrophy, which are physiologic and pathologic cardiac hypertrophy. Unlike pathologic cardiac hypertrophy caused by chronic pressure or volume overload, cardiac hypertrophy induced by exercise is associated with less fibrosis and better systolic function, suggesting that adaptive mechanisms may be involved in exercise-induced cardiac hypertrophy. Therefore, elucidation of the molecular differences between these two types of cardiac hypertrophy may provide insights into the mechanisms underlying the transition from adaptive cardiac hypertrophy to heart failure. By comparing the two types of cardiac hypertrophy, we have identified heat shock transcription factor 1 and its target heat shock proteins as key factors involved in the adaptive mechanism of cardiac hypertrophy. In this review, we summarize the protective role of heat shock transcription factor 1 and heat shock proteins in cardiovascular disease.

• Authors: Haruhiro Toko, Tohru Minamino, Issei Komuro
• Journal: Trends in cardiovascular medicine (Trends Cardiovasc Med) Vol. 18 Issue 3 Pg. 88-93 (Apr 2008) ISSN: 1050-1738 [Print] United States
• PMID: 18436146 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• DNA-Binding Proteins
• HSF1 protein, human
• Heat Shock Transcription Factors
• Heat-Shock Proteins
• Transcription Factors

Topics

• Adaptation, Physiological
• Animals
• Cardiomegaly (metabolism, pathology, physiopathology)
• DNA-Binding Proteins (metabolism)
• Heat Shock Transcription Factors
• Heat-Shock Proteins (metabolism)
• Humans
• Transcription Factors (metabolism)