摘要
自噬是生物进化过程中高度保守、依赖溶酶体的胞内降解途径。在心血管系统中,基础水平的自噬是维持心脏结构和功能稳态的一种机制;在应激状态下,自噬适度激活可保护心肌细胞免受应激损伤,而过度激活则会加重心肌损伤,从而参与多种心血管疾病的病理生理过程。生物体内存在多种自噬调控机制,其中哺乳动物雷帕霉素靶蛋白是自噬的关键负调控因子,研究其介导的自噬在心血管疾病中的作用机制,有助于探索临床预防和治疗心血管疾病的新靶点。
Autophagy is a highly conservative and lysosomal dependent intracellular degradation pathway in the process of biological evolution. In the cardiovascular system,autophagy at the basal level is a mechanism to maintain the homeostasis of heart structure and function. In the state of stress,moderate activation of autophagy can protect cardiomyocytes from stress injury,while excessive activation will aggravate myocardial injury. Thus,autophagy is involved in the pathological process of various cardiovascular diseases. There are a variety of autophagy regulatory mechanisms in organisms,among which mammalian target of rapamycin(mTOR) is a key negative regulator of autophagy. The study on the mechanism of autophagy mediated by m TOR in cardiovascular diseases can provide new strategies for clinical prevention and treatment of cardiovascular diseases.
作者
甘婷
李景东
GAN Ting;LI Jingdong(Department of Cardiology,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,Hubei,China)
出处
《心血管病学进展》
CAS
2020年第4期365-369,共5页
Advances in Cardiovascular Diseases
基金
国家自然科学基金(81873476)。