Galectin-3与心房纤维化的关系及其致心房颤动的机制研究

Atrial fibrillation (AF) was associated with atrial fibrosis. Galectin-3 (Gal-3) is a kind of fibrosis markers related with atrial electrical/structural remodeling and development of AF. Our previous study has found the similar results. Gal-3 can be through a variety of pathways induced myocardial fibrosis. We hypothesized that Gal-3 may participate in the AF by breaking the matrix metalloproteinase/tissue inhibitor of metalloproteinases balance promoting atrial fibrosis, and by maintaining the effects of atrial electrical conduction changes involved in AF.Firstly,the subject AF dog models prove that plasma Gal-3 is associated with atrial fibrosis and AF, and exogenous Gal-3 inhibitor can block the process. Secondly,large sample study proves Gal-3 was associated with AF and recurrence after catheter ablation. Using enzyme-linked immunosorbent assay, Masson staining, echocardiography, Doppler tissue imaging, atrial electrophysiological stimulation and delay of DE-MRI technology. From animal experiment to clinical aspects, it confirmed the hypothesis. This study will elucidate the mechanism of AF induced by Gal-3, and provide a new idea for the upstream for prevention and individual treatment of AF.

心房颤动（房颤）与心房纤维化有关。Galectin-3（Gal-3）是一种纤维化标记物，和心房电/结构重构和房颤发作有关。我们前期小样本临床研究也发现类似结果。Gal-3可以通过多种通路致心肌纤维化作用。我们推测Gal-3可能通过打破基质金属蛋白酶/基质金属蛋白酶组织抑制剂的平衡促进心房纤维化而参与房颤的发生，并通过影响心房电传导的改变参与房颤的维持。本课题采用房颤犬模型证实血浆Gal-3含量与心房纤维化和房颤相关，并利用外源性Gal-3抑制剂阻断上述过程。其次，利用大样本人群验证Gal-3与房颤以及RFCA术后复发的关系。利用酶联免疫吸附测定法、Masson染色、超声心动图、组织多普勒检查、免疫组织化学检查、心房电生理刺激和心脏延迟增强MRI等技术，从动物实验-临床验证两个层面，证实上述假说。本课题将阐明一种全新的Gal-3致房颤机制，为房颤的上游防治和个体化治疗提供新思路。

心房颤动（房颤）与心房纤维化有关。Galectin-3（Gal-3）是一种纤维化标记物，和心房电/结构重构和房颤发作有关。Gal-3可以通过多种通路致心肌纤维化作用。我们推测Gal-3可能通过打破基质金属蛋白酶/基质金属蛋白酶组织抑制剂的平衡促进心房纤维化而参与房颤的发生，并通过影响心房电传导的改变参与房颤的维持。本课题采用房颤犬模型证实血浆Gal-3含量与心房纤维化和房颤相关，并利用外源性Gal-3抑制剂阻断上述过程。其次，利用人群验证Gal-3与房颤以及RFCA术后复发的关系。本课题发现房颤复发患者血浆Gal-3较未复发者明显升高，Gal-3预测房颤RFCA术后复发，阐明了一种全新的Gal-3致房颤机制，为房颤的上游防治和个体化治疗提供新思路。