心梗是造成全球人口“寿命损失”前五大死因之首，其防治手段方法与治疗靶点筛选意义重大。氧化应激是心梗发生发展的核心环节，活性氧导致心磷脂(CL)发生病态重塑，心磷脂重塑酶ALCAT1可调节CL病态重塑，是心血管病发生发展的新靶点。基础与临床研究发现运动改善心功能的机制涉及心肌和血管再生、交感副交感调控、自噬与凋亡等途径，但从心磷脂重塑途径探讨运动改善心梗心脏重塑及其机制研究尚缺。本课题采用ALCAT1-/-小鼠建立心梗模型，进行有氧运动干预；采用ALCAT1过表达和敲除的H9C2细胞低氧培养，以组蛋白去乙酰化酶SIRT1激动剂、抑制剂干预，在整体和细胞、蛋白及分子层面，利用电镜、共聚焦显微镜、荧光免疫组化、WB、RT-qPCR、基因敲入和敲除等技术，探讨有氧运动通过抑制心磷脂重塑酶ALCAT1表达改善心梗心脏功能的机制。为防治心梗手段和方法筛选提供可能靶标和思路，具有重要理论和临床指导意义。

Myocardial infarction (MI) is the primary of five leading causes of death which lead to the loss-of-life in global population. The sifting of prevention means, therapeutic methods and targets will be of great significance. Oxidative stress is the core link of MI occurrence and development. ROS results in the pathological remodeling of cardiolipin (CL). Acyl-CoA:lysocardiolipin acyltransferase-1(ALCAT1), which regulates the pathological remodeling of CL, is a new target of cardiovascular disease occurrence and development. Basic and clinical research found that aerobic exercise can improve heart function significantly, but there is no report about the mechanisms and the relationship between ALCAT1 characterization and heart dysfunction in MI heart. This subject is intended to establish the MI model in ALCAT1 gene knockout mouse and administrate the aerobic exercise intervention; using the ALCAT1 overexpression and interference technology on H9C2 cell culture in hypoxia conditions, which is intervened by the SIRT1 agonist and inhibitor in order to investigate the ALCAT1 characterization and whether aerobic exercise improves the heart function through ALCAT1 in MI heart in vivo and in vitro, as well as the related signaling mechanism by multi- techniques such as electron microscope, confocal, immunofluorescence, WB, RT-qPCR, gene overexpression and knockout in the levels of tissue, cell, protein and molecular. Providing the possible targets and ideas on the sifting of prevention means and therapeutic methods in MI caused heart failure has the important theoretical and clinical guiding significance.