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Novel insights: Dynamic foam cells derived from the macrophage in atherosclerosis
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2021-01-28 , DOI: 10.1002/jcp.30300
Jun Li 1 , Qinghai Meng 1 , Yu Fu 1 , Xichao Yu 1 , Tingting Ji 1 , Ying Chao 1 , Qi Chen 1 , Yu Li 2 , Huimin Bian 1, 3
Affiliation  

Atherosclerosis can be regarded as a chronic disease derived from the interaction between disordered lipoproteins and an unsuitable immune response. The evolution of foam cells is not only a significant pathological change in the early stage of atherosclerosis but also a key stage in the occurrence and development of atherosclerosis. The formation of foam cells is mainly caused by the imbalance among lipids uptake, lipids treatment, and reverse cholesterol transport. Although a large number of studies have summarized the source of foam cells and the mechanism of foam cells formation, we propose a new idea about foam cells in atherosclerosis. Rather than an isolated microenvironment, the macrophage multiple lipid uptake pathways, lipid internalization, lysosome, mitochondria, endoplasmic reticulum, neutral cholesterol ester hydrolase (NCEH), acyl-coenzyme A–cholesterol acyltransferase (ACAT), and reverse cholesterol transport are mutually influential, and form a dynamic process under multi-factor regulation. The macrophage takes on different uptake lipid statuses depending on multiple uptake pathways and intracellular lipids, lipid metabolites versus pro-inflammatory factors. Except for NCEH and ACAT, the lipid internalization of macrophages also depends on multicellular organelles including the lysosome, mitochondria, and endoplasmic reticulum, which are associated with each other. A dynamic balance between esterification and hydrolysis of cholesterol for macrophages is essential for physiology and pathology. Therefore, we propose that the foam cell in the process of atherosclerosis may be dynamic under multi-factor regulation, and collate this study to provide a holistic and dynamic idea of the foam cell.

中文翻译:

新见解:源自动脉粥样硬化巨噬细胞的动态泡沫细胞

动脉粥样硬化可以被认为是一种由紊乱的脂蛋白和不适当的免疫反应之间相互作用引起的慢性疾病。泡沫细胞的进化不仅是动脉粥样硬化早期的显着病理变化,也是动脉粥样硬化发生发展的关键阶段。泡沫细胞的形成主要是由于脂质摄取、脂质处理和胆固醇逆向转运失衡所致。尽管大量研究总结了泡沫细胞的来源和泡沫细胞形成的机制,但我们对动脉粥样硬化中的泡沫细胞提出了新的观点。巨噬细胞不是孤立的微环境,而是多种脂质摄取途径、脂质内化、溶酶体、线粒体、内质网、中性胆固醇酯水解酶 (NCEH)、酰基辅酶A-胆固醇酰基转移酶(ACAT)与胆固醇逆向转运相互影响,在多因素调控下形成动态过程。巨噬细胞呈现不同的摄取脂质状态,具体取决于多种摄取途径和细胞内脂质、脂质代谢物与促炎因子。除 NCEH 和 ACAT 外,巨噬细胞的脂质内化还依赖于多细胞器,包括溶酶体、线粒体和内质网,它们相互关联。巨噬细胞的胆固醇酯化和水解之间的动态平衡对于生理学和病理学至关重要。因此,我们提出动脉粥样硬化过程中的泡沫细胞可能在多因素调控下是动态的,
更新日期:2021-01-28
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