心肌纤维化与AMPK-mTOR-ULK1信号通路研究进展
Research progress of myocardial fibrosis and AMPK-mTOR-ULK1 signaling pathway
摘要心肌纤维化是诸多心血管疾患发生发展的重要病理变化,也是造成心脏泵衰竭及不良心血管事件的病理基础,其主要表现为细胞外基质(ECM)的过度沉积与成纤维细胞(CFs)的不断增殖。腺苷酸活化蛋白激酶(AMPK)信号通路是介导磷酸化的主要系统,AMPK激活自噬,可抑制雷帕霉素靶蛋白(mTOR),也可磷酸化Unc-51样自噬激活激酶1(ULK1);AMPK信号通路在心肌纤维化的发生发展过程中起到了重要作用,本文通过分析AMPK-mTOR-ULK1信号通路在心肌纤维化中的作用,以期为心肌纤维化的治疗提供指导。
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abstractsMyocardial fibrosis is an important pathological change in the occurrence and development of many cardiovascular diseases, and it is also the pathological basis of heart pump failure and adverse cardiovascular events, which is mainly manifested by excessive deposition of extracellular matrix (ECM) and continuous proliferation of cardiac fibroblasts (CFs). Adenylate activated protein kinase (AMPK) signaling pathway is the main system to mediate phosphorylation. AMPK activates autophagy, inhibits mammalian target of rapamycin (mTOR), and phosphorylates Unc-51-like autophagy activated kinase 1(ULK1). AMPK signaling pathway plays an important role in the occurrence and development of myocardial fibrosis. This paper analyzes the role of AMPK-mTOR-ULK1 signaling pathway in myocardial fibrosis, hoping to provide guidance for the treatment of myocardial fibrosis.
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