摘要
主动脉瓣钙化是一种由多种因素共同参与的与年龄相关的复杂病理性改变,晚期可致主动脉瓣狭窄,严重影响患者生活质量。炎症被认为是导致主动脉瓣钙化的因素之一。单核细胞的浸润与巨噬细胞的极化是主动脉瓣膜炎症发生发展的重要机制。活化的巨噬细胞产生肿瘤坏死因子-α、白介素-1β等细胞因子,并通过分泌基质降解酶重塑细胞外基质加速瓣膜钙化。巨噬细胞也可以通过吸收脂质分化为泡沫细胞参与钙化进程。此外,单核细胞与其他免疫细胞的相互作用也对主动脉瓣钙化具有一定的影响。现通过查阅相关文献,就单核/巨噬细胞与主动脉瓣钙化发生发展的相关机制做一综述。
Aortic valve calcification is an age-related complicated pathological process involving multiple factors,and may result in valve stenosis in the late stage and decrease the life quality of patients.Inflammation is considered as one of the factors which may lead to aortic valve calcification.The infiltration of monocytes and the polarization of macrophages are important mechanisms for the occurrence and development of aortic valve inflammation.Activated macrophages produce cytokines such as tumor necrosis factor-αand interleukin-1β,and reshape extracellular matrix by secreting matrix degradation enzymes to accelerate valve calcification.Macrophage also differentiate into foam cells by absorbing lipids to participate in the calcification process.In addition,differentiation of monocytes into other immune cells also contribute a certain effect on aortic valve calcification.Our review summarizes the related mechanisms of monocytes and macrophages involving in the occurrence and development of aortic valve calcification.
作者
陈乾
秦铭
徐志云
CHEN Qian;QIN Ming;XU Zhiyun(College of Basic Medical Sciences,The People’s Liberation Army Naval Medical University,Shanghai 200433,China;Department of Cardiac Surgery,Changhai Hospital,Naval Medical University,Shanghai 200433,China)
出处
《心血管病学进展》
CAS
2022年第10期898-901,共4页
Advances in Cardiovascular Diseases
基金
国家自然科学基金面上项目(81870287)。