心房纤维化在心房颤动（房颤）的自然病程以及房颤患者导管消融术（RFA）后的复发中起关键作用，但具体机制不明。前期工作中我们建立了国内最大样本量的房颤临床资源与样本库，初步勾勒出我国房颤的流行病学和临床特征。我们的前瞻性临床试验首次证实，血浆高Galectin-3（Gal-3）水平与房颤患者RFA术后复发相关，既往研究证明，Gal-3是肝、肺、肾等组织纤维化发生发展的重要分子节点，据此提出“Gal-3是心房纤维化重要分子开关”的核心假说。本项目立足于前期研究基础，以房颤心房纤维化的自然病程和房颤RFA造成的医源性心房纤维化这两个临床问题为切入点，建立以Gal-3为核心的房颤-心房纤维化表型组学，明确Gal-3在房颤临床转归中的作用；在动物模型上研究Gal-3致心房纤维化的机制；探索Gal-3抑制能否延缓甚至逆转心房纤维化。籍此为建立以Gal-3为靶点的房颤防治和术后复发防范策略提供科学依据。

Atrial fibrosis plays an important role in the natural progression of atrial fibrillation (AF) and the recurrence of AF after radiofrequency catheter ablation in the patients with AF, but the underlying mechanisms are unknown. So far we have established the largest biobank of AF in China and preliminarily have delineated the epidemiological and clinical characteristics of patients with AF in our country. Based on the biobank, we demonstrated that Galectin-3, a biomarker of fibrosis, was associated with the recurrence of AF after radiofrequency catheter ablation in the patients with AF; many studies in other tissues have demonstrated that Galectin-3 play a critical role in the fibrogenesis, thus we propose that Galectin-3 is a key molecular point in the atrial fibrosis. In this project, Aim 1: we plan to establish the atrial fibrillation-atrial fibrosis phenomics with the focusing on the Galectin-3 and its associated biomarks. Aim 2: we plan to investigate the underlying mechanisms for the Galectin-3 associated atrial fibrosis. Aim 3: we plan to explore the inhibition of Galectin-3 to delay or reverse of atrial fibrosis. Taken together, this project is to establish Galectin-3 as a novel target for the prevention and treatment of atrial fibrillation.