脂肪组织
衰老
脂肪细胞
生物
细胞生物学
人口
干细胞
适应不良
内分泌学
内科学
医学
遗传学
环境卫生
作者
Zixin Zhou,Huiying Zhang,Yan Tao,Haipeng Jie,Jinshi Zhao,Jinhao Zang,Huijie Li,Yalin Wang,Tianci Wang,Hui Zhao,Yuan Li,Chun Guo,Faliang Zhu,Hongzhi Mao,Lining Zhang,Fengming Liu,Qun Wang
出处
期刊:Cell Reports
[Elsevier]
日期:2023-05-01
卷期号:42 (5): 112424-112424
被引量:6
标识
DOI:10.1016/j.celrep.2023.112424
摘要
Adipose-derived stem cells (ASCs) drive healthy visceral adipose tissue (VAT) expansion via adipocyte hyperplasia. Obesity induces ASC senescence that causes VAT dysfunction and metabolic disorders. It is challenging to restrain this process by biological intervention, as mechanisms of controlling VAT ASC senescence remain unclear. We demonstrate that a population of CX3CR1hi macrophages is maintained in mouse VAT during short-term energy surplus, which sustains ASCs by restraining their senescence, driving adaptive VAT expansion and metabolic health. Long-term overnutrition induces diminishment of CX3CR1hi macrophages in mouse VAT accompanied by ASC senescence and exhaustion, while transferring CX3CR1hi macrophages restores ASC reservoir and triggers VAT beiging to alleviate the metabolic maladaptation. Mechanistically, visceral ASCs attract macrophages via MCP-1 and shape their CX3CR1hi phenotype via exosomes; these macrophages relieve ASC senescence by promoting the arginase1-eIF5A hypusination axis. These findings identify VAT CX3CR1hi macrophages as ASC supporters and unravel their therapeutic potential for metabolic maladaptation to obesity.
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