Latronico Michael V G, Elia Leonardo, Condorelli Gianluigi, Catalucci Daniele
Laboratory of Molecular Cardiology, Scientific and Technology Pole, IRCCS MultiMedica Hospital, 20138 Milan, Italy.
Int J Biochem Cell Biol. 2008;40(9):1643-8. doi: 10.1016/j.biocel.2008.03.002. Epub 2008 Mar 18.
Heart failure (HF) is a syndrome caused by diminished heart function that arises from pathologies like hypertension, infarction, and diabetes. Neurohormonal, cardiorenal and cardiocirculatory models have been developed to explain HF but they have not provided sufficient understanding for the elaboration of therapies to conquer the syndrome. In fact, even though progress has been made in improving survival, HF remains a frequent cause of hospitalization and death. Since in most forms of HF, development of the disorder is associated with an alteration of cardiomyocyte structure, perceived as an increase in heart mass due to cell hypertrophy, effort is being directed to address hypertrophy as a therapeutic target. Here, we outline recent understanding of two gene-silencing regulatory mechanisms underlying cardiomyocyte hypertrophy, i.e., transcriptional control by HDACs, and post-transcriptional control by microRNAs.
心力衰竭（HF）是一种由心脏功能减退引起的综合征，其源于高血压、梗死和糖尿病等病理状况。人们已建立神经激素、心肾和心脏循环模型来解释心力衰竭，但这些模型尚未为攻克该综合征的治疗方法阐述提供足够的理解。事实上，尽管在提高生存率方面已取得进展，但心力衰竭仍是住院和死亡的常见原因。由于在大多数形式的心力衰竭中，疾病的发展与心肌细胞结构的改变相关，这种改变表现为由于细胞肥大导致的心脏质量增加，因此人们正致力于将肥大作为治疗靶点。在此，我们概述了对心肌细胞肥大背后两种基因沉默调控机制的最新认识，即组蛋白去乙酰化酶（HDACs）的转录控制和微小RNA的转录后控制。
