1.1)四川省肿瘤医院肿瘤放射治疗科,成都 610041;2.2)四川大学华西基础医学与法医学院生物医学工程实验室,成都 610041
Tel:
国家自然科学基金
1.1)Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610041, China;2.2)Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China
The National Natural Science Foundation of China
心血管疾病中动脉粥样硬化斑块的钙化是动脉粥样硬化的临床标志之一,主要发生在动脉血管的内膜。动脉粥样硬化斑块核心的钙化不会增加斑块的易损性,而粥样斑块纤维帽上的微钙化会加强纤维帽的周向应力,致使斑块的易损性增加。动脉粥样硬化斑块的钙化机制包括被动钙化和主动钙化,被动钙化受激素和局部信号的调节,主动钙化机制涉及复杂的细胞生命过程,基质囊泡、细胞凋亡、外泌体、氧化应激反应和细胞自噬等均参与了钙化过程。本文对动脉粥样硬化斑块的钙化机制的进展进行综述。
Calcification of atherosclerotic plaque, which mainly observed in the intima of arterial vessels, is one of the clinical signs of atherosclerosis in cardiovascular diseases. Calcification in atheroma dose not increase the vulnerability of plaque, while microcalcification (μCalcs) located within the fibrous cap could intensify the background circumferential stress in the cap, resulting in increased vulnerability of plaque. The mechanisms of calcification in atherosclerotic plaques include passive calcification and active calcification. Passive calcification is regulated by hormones and local signals. The mechanisms of active calcification are a cell-mediated process, participated by matrix vesicles, cell apoptosis, exosomes, oxidative stress response and autophagy. This paper reviews the calcification mechanisms of atherosclerotic plaque.
姚杏红,邱艳,曾烨,李良.动脉粥样硬化斑块钙化机制的研究进展[J].生物化学与生物物理进展,2020,47(7):574-581
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