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Mitochondrial metabolism in regulating macrophage polarization: an emerging regulator of metabolic inflammatory diseases.
Acta Biochimica et Biophysica Sinica ( IF 3.3 ) Pub Date : 2020-08-12 , DOI: 10.1093/abbs/gmaa081
Jina Qing 1, 2 , Zizhen Zhang 3 , Petr Novák 1 , Guojun Zhao 4 , Kai Yin 1, 2
Affiliation  

As a major type of immune cells with heterogeneity and plasticity, macrophages are classically divided into inflammatory (M1) and alternative/anti-inflammatory (M2) types and play a crucial role in the progress of the inflammatory diseases. Recent studies have shown that metabolism is an important determinant of macrophage phenotype. Mitochondria, one of the most important compartments involving cell metabolism, are closely associated with the regulation of cell functions. In most types of cell, mitochondrial oxidative phosphorylation (OXPHOS) is the primary mode of cellular energy production. However, mitochondrial OXPHOS is inhibited in activated M1 macrophages, rendering them unable to be converted into M2 phenotype. Thus, mitochondrial metabolism is a crucial regulator in macrophage functions. This review summarizes the roles of mitochondria in macrophage polarization and analyzes the molecular mechanisms underlying mitochondrial metabolism and function, which may provide new approaches for the treatment of metabolic inflammatory diseases.

中文翻译:

线粒体代谢在调节巨噬细胞极化中的作用:代谢性炎症疾病的新兴调节剂。

作为具有异质性和可塑性的主要免疫细胞类型,巨噬细胞通常分为炎性(M1)和替代/抗炎(M2)类型,并且在炎性疾病的进展中起着至关重要的作用。最近的研究表明,代谢是巨噬细胞表型的重要决定因素。线粒体是涉及细胞代谢的最重要的区室之一,与细胞功能的调节密切相关。在大多数类型的细胞中,线粒体氧化磷酸化(OXPHOS)是细胞产生能量的主要方式。然而,线粒体OXPHOS在激活的M1巨噬细胞中被抑制,使其无法转化为M2表型。因此,线粒体代谢是巨噬细胞功能的关键调节器。
更新日期:2020-09-14
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