心肌肥厚是高血压导致的心脏重要病理改变之一，研究其发生机制对高血压心脏病的治疗有重要意义。Ddx17在心肌表达十分丰富，但其功能目前尚不清楚。我们研究发现：Ddx17在心肌肥厚发生时表达增高；小鼠Ddx17心肌特异性敲除可以减轻血管紧张素II诱导的心肌肥厚；而过表达Ddx17可以导致心肌细胞肥大发生。通过免疫共沉淀和蛋白质质谱分析，我们发现Ddx17可以与雌激素相关受体α结合，并降低下游心肌肥厚抑制基因的表达。据此我们提出假说：Ddx17可能通过ERRα调控下游基因表达，促进心肌细胞肥厚的发生。本研究拟从分子、细胞和整体水平，利用心肌细胞模型、患者和小鼠心脏病理标本、Ddx17心肌特异性敲除或过表达小鼠，以实时定量RT-PCR、免疫组化、蛋白质免疫共沉淀等方法，探讨Ddx17在心肌肥厚发生中的功能和作用。本研究将从Ddx17这个新视点为揭示心肌肥厚的发生机制，为心肌肥厚的防治提供新思路。

Heart hypertrophy is one of the major pathological changes of hypertension. It is important to investigate the regulation mechanisms of heart hypertrophy for the treatment of cardiovascular diseases. Ddx17 is a transcription co-regulator mainly expressed in cardiomyocyte. But its function in cardiovascular system is still not clear. Our previous study found that Ddx17 was up regulated during the development of heart hypertrophy. Ddx17 cardiomyocyte specific knockout in adult mouse could attenuate Angiotensin II induced heart hypertrophy in vivo. And overexpression of Ddx17 by adenovirus vector could induce cardiomyocyte hypertrophy in vitro. We also found that Ddx17 could bind to transcription factor ERRα by co-immunoprecipitation and protein mass spectrometry，and inhibit some anti-hypertrophic gene expression in cardiomyocyte. Thus, we hypothesize that Ddx17 could promote heart hypertrophy by regulating ERRα and its downstream signal pathways. We will use cultured cardiomyocyte, human and mouse heart hypertrophy sample, Ddx17 cardiomyocyte specific knockout mouse, Ddx17 cardiomyocyte specific overexpression mouse, to investigate Ddx17’s role by real-time RT-PCR, immunohistochemistry and co-immunoprecipitation in molecular, cellular, tissue and animal levels during the development of heart hypertrophy. The study will reveal a new mechanism for Ddx17 during the development of heart hypertrophy and provide a new insight for the prevention and treatment of heart diseases.