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Research progress on the regulatory mechanism of myocardial regeneration after myocardial infarction#br# |
MA Yifu1,2 LIU Tingting1,2 SUN Fangling1,2 TIAN Xin1,2 WANG Yufeng1,2 ZHENG Ruifang3 XING Jianguo3 WANG Wen1,2,3,4▲ |
1.Laboratory Animal Room, Xuanwu Hospital, Capital Medical University, Beijing 100053, China;
2.Beijing Municipal Geriatric Medical Research Center, Beijing 100053, China;
3.Institute of Medicine of Xinjiang Uygur Autonomous Region, Xinjiang Uygur Autonomous Region, Urumqi 830002, China;
4.Beijing Institute of Major Brain Disorders,Beijing 100069, China |
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Abstract After myocardial infarction, the tissue is ischemic and hypoxic, and a large number of myocardial cells in the infarction area are necrotic, and the damaged tissue is replaced by fibrotic cells, forming scar tissue. Remodeling of the ventricular wall in the non-infarcted area leads to a decrease in the ability of the heart muscle to contract, ultimately leading to heart failure. According to the latest report of the World Health Organization, myocardial infarction and other cardiovascular diseases are the leading causes of death worldwide. In recent years, the problem of younger patients with myocardial infarction has become increasingly prominent, and the overall mortality is on the rise. Myocardial regeneration is a process in which the original myocardial cells proliferate a little after myocardial infarction to alleviate the injury caused by myocardial infarction. Studies have shown that myocardial regeneration after myocardial infarction can be promoted by promoting the self-replication of myocardial cells. In this paper, the current research progress on endogenous repair of myocardial infarction is summarized, and microRNA and cytokines are discussed to induce myocardial cells to re-enter the cell cycle and realize the proliferation of myocardial cells through some specific signaling pathways. In order to find a new way to treat myocardial infarction, this paper reviews the existing regulation mechanism of myocardial regeneration.
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