心肌肥厚的发生机制之一是蛋白质合成和降解失衡，持续刺激使心肌蛋白质合成信号过度激活或蛋白质降解减低则可促进心肌肥厚的发生。Maf1是RNA聚合酶III的抑制物，可通过抑制RNA聚合酶III抑制转录，从而减少蛋白质合成。然而，目前尚无Maf1与心肌肥厚关系的研究报道。我们发现，利用小干扰RNA沉默Maf1可明显促进苯肾上腺素诱导的心肌细胞肥厚，并且，通过重组腺病毒转染过表达Maf1对心肌肥厚有显著的抑制作用，提示Maf1可能在心肌肥厚的过程中起重要的调控作用。因此，为深入研究Maf1对心肌肥厚的调控机制，本研究拟通过心脏特异性Maf1转基因小鼠、重组腺病毒转染过表达和基因沉默Maf1以评价Maf1在压力过负荷和苯肾上腺素诱导的心肌肥厚中的作用，并深入分析Maf1在心肌肥厚中对转录通路的影响及作用位点，旨在阐明Maf1调控心肌肥厚的核心机制，为寻找心肌肥厚的临床治疗新靶点提供理论依据。

The imbalance between protein synthesis and degradation is one of the mechanisms of cardiac hypertrophy, consistent pro-hypertrophic stimulus could induce the sigalings of protein synthesis or impair protein degradation, which will result in the development of cardiac hypertrophy.A potent RNA polymerase III inhibitor, Maf1, which blocks transcription through inhibiting RNA polymerase III, could result in decreased protein synthesis. There is no study related to Maf1 and cardiac hypertrophy, in our pilot study, we found silencing Maf1 by siRNA could significantly stimulate phenylephrin induced cardiac hypertrophy, moreover, greatly reduced hypertrophy was found in cardiomyocytes with overexpressed Maf1 by adenovirus transfection, suggesting Maf1 may play an important role in the development of cardiac hypertrophy. Therefore, in the present study, with cardiac specific Maf1 transgenic mouse, recombinated adenovirus and siRNA, we aim to further elucidate the effects and mechanisms of Maf1 inhibiting cardiac hypertrophy in pressure overload and phenylephrin induced hypertrophic models in vivo and in vitro, explore the effect of Maf1 on transcription as well as possible targets and clarify the core mechanism of Maf1 regulating hypertrophy. Consequently, the present study could further the research of molecular mechanisms in cardiac hypertrophy and provide proofs for new treating targets of cardiac hypertrophy.