Toko Haruhiro, Minamino Tohru, Komuro Issei
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, Japan.
Trends Cardiovasc Med. 2008 Apr;18(3):88-93. doi: 10.1016/j.tcm.2008.01.003.
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.
心脏肥大是心血管疾病的独立危险因素。最初,心脏肥大是对壁应力增加的适应性反应,但持续的压力会导致心力衰竭。目前尚不清楚从适应性心脏肥大向失适应性心脏肥大的转变是如何发生的。据推测,心脏肥大有两种形式,即生理性和病理性心脏肥大。与由慢性压力或容量超负荷引起的病理性心脏肥大不同,运动诱导的心脏肥大与较少的纤维化和较好的收缩功能相关,这表明适应性机制可能参与运动诱导的心脏肥大。因此,阐明这两种类型心脏肥大之间的分子差异可能有助于深入了解从适应性心脏肥大向心力衰竭转变的潜在机制。通过比较这两种类型的心脏肥大,我们已确定热休克转录因子1及其靶标热休克蛋白是参与心脏肥大适应性机制的关键因素。在本综述中,我们总结了热休克转录因子1和热休克蛋白在心血管疾病中的保护作用。