心肌肥厚与纤维化导致的心室重构是心力衰竭发生发展的重要因素，蛋白质合成和降解失衡为引起心室重构的主要机制之一。在前期研究中，我们在心肌细胞中利用重组腺病毒转染过表达和基因沉默Maf1均证实Maf1可明显抑制心肌肥厚，此效应与Maf1抑制RNA聚合酶III、抑制转录、减少蛋白质合成相关。并且，在压力过负荷诱导的心力衰竭中，利用心脏特异性过表达Maf1转基因小鼠，我们发现过表达Maf1明显改善心力衰竭，伴随着降低的心肌肥厚与心肌纤维化，同时心脏自噬水平升高。因此，为深入研究Maf1对心力衰竭的调控机制，本研究拟通过心脏特异性过表达Maf1转基因小鼠和腺病毒转染过表达Maf1，从动物和细胞水平探讨Maf1对心室重构的调控作用，并深入分析其机制，旨在阐明Maf1调控转录、降低蛋白质合成与促进自噬、提高蛋白质降解是否为其抑制心室重构、拮抗心力衰竭的核心机制，为心力衰竭的临床治疗提供新靶点和理论依据。

One of the most important factors in the development of heart failure is ventricular remodeling which resulted from cardiac hypertrophy and fibrosis. The imbalance between protein synthesis and degradation in cardiomyocytes is a pivotal mechanism for remodeling progression.In our previous study,with adenoviral transfection and silencing of Maf1, we proved Maf1 could significantly inhibit cardiac hypertrophy, the effect related to that Maf1 can block RNA polymerase III, repress transcription so as to inhibit protein synthesis finally. Moreover, in cardiac specific Maf1 transgenic mice, we found overexpressed Maf1 could improve heart failure,decrease hypertrophy and fibrosis induced by pressure overload, with enhanced autophagy level.Therefore,in the present study,we aim to further the research of molecular mechanisms in heart failure and?explore the role of Maf1 in remodeling in vivo and in vitro, in order to elucidate whether blocking protein synthesis by transcription inhibition and inducing protein degradation by autophagy are key mechanisms of Maf1 repressing remodeling as well as improving heart failure. Consequently,the present study could provide proofs for new treating targets of heart failure.