Medical Department III-Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Germany Liebigstr. 20, 04103 Leipzig, Germany.
Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG), Helmholtz Zentrum München, University of Leipzig and University Hospital Leipzig, 04103 Leipzig, Germany.
Int J Mol Sci. 2021 Feb 2;22(3):1500. doi: 10.3390/ijms22031500.
The mechanisms of how obesity contributes to the development of cardio-metabolic diseases are not entirely understood. Obesity is frequently associated with adipose tissue dysfunction, characterized by, e.g., adipocyte hypertrophy, ectopic fat accumulation, immune cell infiltration, and the altered secretion of adipokines. Factors secreted from adipose tissue may induce and/or maintain a local and systemic low-grade activation of the innate immune system. Attraction of macrophages into adipose tissue and altered crosstalk between macrophages, adipocytes, and other cells of adipose tissue are symptoms of metabolic inflammation. Among several secreted factors attracting immune cells to adipose tissue, chemotactic C-C motif chemokine ligand 2 (CCL2) (also described as monocyte chemoattractant protein-1 (MCP-1)) has been shown to play a crucial role in adipose tissue macrophage infiltration. In this review, we aimed to summarize and discuss the current knowledge on CCL2 with a focus on its role in linking obesity to cardio-metabolic diseases.
肥胖如何导致心脏代谢疾病的发生机制尚不完全清楚。肥胖常伴有脂肪组织功能障碍，其特征为脂肪细胞肥大、异位脂肪堆积、免疫细胞浸润和脂肪因子分泌改变。脂肪组织分泌的因子可能诱导和/或维持固有免疫系统的局部和全身低度激活。巨噬细胞向脂肪组织的募集以及巨噬细胞、脂肪细胞和脂肪组织中其他细胞之间的异常相互作用是代谢炎症的表现。在吸引免疫细胞进入脂肪组织的几种分泌因子中，趋化因子 C-C 基序趋化因子配体 2（CCL2）（也称为单核细胞趋化蛋白-1（MCP-1））已被证明在脂肪组织巨噬细胞浸润中发挥关键作用。在这篇综述中，我们旨在总结和讨论 CCL2 的现有知识，重点关注其将肥胖与心脏代谢疾病联系起来的作用。
