长链非编码RNA-Gm14005通过Bif-1调控线粒体分裂和心肌肥大的作用及机制研究

心肌细胞肥大是心血管疾病中最常见的心肌细胞病理变化之一，而心肌肥厚持续进展最终会导致心力衰竭和猝死。线粒体作为细胞内的功能细胞器，其动态平衡在心血管疾病的发病过程中扮演了重要的角色。课题组前期研究结果表明lncRNA-Gm14005和Bif-1在心肌肥大的过程中显著上调，具有促进线粒体分裂和心肌细胞肥大的作用。据此，本项目拟研究Gm14005和Bif-1的相互作用及其调节线粒体分裂和心肌肥大的分子机制。具体内容包括：1.Bif-1在线粒体分裂和心肌肥大中的作用；2.Gm14005和Bif-1的相互作用和分子机制；3.Gm14005在线粒体分裂和心肌肥大中的作用。目的寻找到由Bif-1介导的lncRNA-Gm14005参与调控线粒体分裂和心肌肥大的新途径。本研究将为阐明线粒体动态平衡相关分子在心脏肥厚疾病中的作用及机制提供理论依据，为心脏疾病的预防、治疗提供新靶点。

Myocardial hypertrophy is one of the most common pathological changes of cardiomyocytes in cardiovascular disease, and sustained cardiac hypertrophy eventually leads to heart failure and sudden death. As a functional intracellular organelle, the dynamic balance of mitochondria plays an important role in the pathogenesis of cardiovascular disease. Our previous results showed that lncRNA-Gm14005 and Bif-1 were significantly up-regulated during cardiac hypertrophy. They could promote mitochondrial fission and myocardial hypertrophy. Accordingly, this project intends to study the molecular mechanism of the interaction of Gm14005 and Bif-1 to regulate mitochondrial fission and myocardial hypertrophy. The specific research contents include: 1.to study the role of Bif-1 in mitochondrial fission and myocardial hypertrophy; 2.to study the interaction and molecular mechanism of Gm14005 and Bif-1; 3.to study the role of Gm14005 in mitochondrial fission and myocardial hypertrophy. This project aims to reveal a new pathway of lncRNA-Gm14005 mediated by Bif-1 to regulate mitochondrial fission and myocardial hypertrophy.This study will provide a theoretical basis for elucidating the role and mechanism of mitochondrial homeostasis related molecules in cardiac hypertrophy and provide new targets for the prevention and treatment of heart disease.