| Autor: |
Zhou, Zixin, Zhang, Huiying, Tao, Yan, Jie, Haipeng, Zhao, Jingyuan, Zang, Jinhao, Li, Huijie, Wang, Yalin, Wang, Tianci, Zhao, Hui, Li, Yuan, Guo, Chun, Zhu, Faliang, Mao, Haiting, Zhang, Lining, Liu, Fengming, Wang, Qun |
| Zdroj: |
Cell Reports; 20230101, Issue: Preprints |
| Abstrakt: |
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 challengeable to restrain this process by biological intervention, as mechanisms of controlling VAT ASC senescence remain unclear. We demonstrate that a population of CX3CR1himacrophages 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 CX3CR1himacrophages in mouse VAT accompanied by ASC senescence and exhaustion, while transferring CX3CR1himacrophages restores ASC reservoir and triggers VAT beiging to alleviate the metabolic maladaptation. Mechanistically, visceral ASCs attract macrophages via MCP-1 and shape their CX3CR1hiphenotype via exosomes; these macrophages relieve ASC senescence by promoting the arginase1-eIF5A hypusination axis. These findings identify VAT CX3CR1himacrophages as ASC supporters and unravel their therapeutic potential for metabolic maladaptation to obesity. |
| Databáze: |
Supplemental Index |
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