房颤患者心外膜脂肪组织通过旁分泌蛋白HSP47促进成纤维细胞胶原分泌的机制研究

心房纤维化的形成是房颤形成基本且重要的机制，既往研究发现心外膜脂肪组织（EAT）对心房纤维化的形成和发展有重要影响，但是房颤患者EAT脂肪类型及影响心房纤维化的机制尚不明确。.课题组前期发现51例房颤患者的心外膜脂肪组织中既存在棕色脂肪，又呈现出白色脂肪的特性，而非既往认为的单一棕色脂肪细胞成份，提示房颤患者的心外膜脂肪出现棕色向白色转化的表型重构。对EAT的旁分泌蛋白的行KEGG、GO聚类分析发现房颤患者心外膜脂肪组织分泌的热休克蛋白(HSP47)明显升高，但EAT旁分泌的HSP47在心房纤维化形成过程中的功能尚不明确。.本课题组拟系统探讨房颤疾病状态下的心外膜脂肪的重构分型以及和非房颤患者EAT分泌蛋白谱的变化；进而通过GO和KEGG聚类分析探究其差异旁分泌蛋白HSP47参与心房纤维化的可能分子机制，进一步揭示房颤患者心外膜脂肪与心房纤维化的关系，为房颤疾病的治疗提供新的靶标。

The formation of atrial fibrosis is the most basic and essential mechanism for the construction in atrial fibrillation (AF). Meanwhile, previous studies have found that epicardial adipose tissue (EAT) played a key role in development and progression of atrial fibrosis. However, it remains to be elucidated about the type of EAT in patients with AF and its mechanism how EAT influences atrial fibrosis..Previous study reported that EAT was a single component of brown fat. However, our previous research found that EAT contained not only brown adipocyte but also white adipocyte in 51 patients with AF. Moreover, our finding suggested that there was a trend in phenotypic remodeling from brown to white conversion in EAT in patients with AF. The KEGG and GO cluster analysis of the paracrine protein of EAT found that the heat shock protein (HSP47) secreted by the EAT in AF patients was significantly higher than patients without AF. However, the function of the paracrine HSP47 of EAT in the formation of atrial fibrosis is still unknown..Our research aims to systematically explore the remodeling classification of epicardial fat in AF patients and the changes of EAT secreted protein profile in patients with or without AF. And then, we explore the possible molecular mechanism how the differential paracrine protein HSP47 participates in atrial fibrosis through GO and KEGG cluster analysis. Furthermore, we could reveal the relationship between EAT and atrial fibrosis in AF patients and provide a new therapeutic target for the treatment and prevention of AF.