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Editorial
. 2008 Nov 21;103(11):1194-6.
doi: 10.1161/CIRCRESAHA.108.189118.

A new (heat) shocking player in cardiac hypertrophy

Thomas M Vondriska, Yibin Wang
Editorial

A new (heat) shocking player in cardiac hypertrophy

Thomas M Vondriska et al. Circ Res. .

Abstract

Hypertrophic growth of cardiac myocytes is a common result of different physiological and pathological stresses. It remains a subject of considerable debate whether hypertrophy is a compensatory process that becomes maladaptive in diseased hearts or a direct contributor to the pathogenesis of heart failure. Nevertheless, many types of stressors, mechanical or neural/hormonal, induce hypertrophy and this phenoytpe is an independent risk factor in heart failure. Therefore, much effort has been devoted to uncovering mechanisms of hypertrophic growth with the expectation that intercepting this process clinically may halt the disease progression of heart failure. It is firmly established that hypertrophic growth involves alterations in gene regulation, excitation-contractile coupling, extracellular matrix remodeling and energy metabolism.

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Figures

Figure
Figure. Distinct roles of HDACs to regulate cardiac hypertrophy
Various hypertrophic stressors are known to induce class II HDACs by promoting their relocalization from nucleus to cytoplasm, thereby removing their inhibition of pro-hypertrophic cardiac transcription. Recent studies, including those examined in the paper by Kee and colleagues, suggest an alternative mechanism for the participation of the class I HDAC2 in hypertrophy. In this scenario, hypertrophic stressors induce association of HDAC2 with Hsp70, leading to repression of anti-hypertrophic genes. The arrows and lines depict positive or negative functions without implication of direct interactions.
See this image and copyright information in PMC

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