School of Life Sciences, Anhui University of Chinese Medicine, 350 Longzihu Road, Xinzhan District, Hefei 230012, China.
School of Life Sciences, Hainan University, 58 Renmin Avenue, Meilan District, Haikou 570228, China.
Oxid Med Cell Longev. 2021 Aug 30;2021:9980877. doi: 10.1155/2021/9980877. eCollection 2021.
Adipose tissue macrophages (ATM) are a major source of low-grade inflammation in obesity, and yet reasons driving ATM accumulation in white adipose tissue (WAT) are not fully understood. Emerging evidence suggested that ATM underwent extensive remodeling in obesity. In addition to abundance, ATM in obesity were lipid-laden and metabolically reprogrammed, which in turn was tightly related to their functional alterations and persistence in obesity. Herein, we aimed to discuss that activation of lipid sensing signaling associated with metabolic reprogramming in ATM was indispensible for their migration, retention, or proliferation in obesity. Likewise, lipolysis also induced similar but transient ATM remodeling. Therefore, we assumed that obesity might share overlapping mechanisms with lipolysis in remodeling ATM. Formation of crown-like structures (CLS) in WAT was presumably a common event initiating ATM remodeling, with a spectrum of lipid metabolites released from adipocytes being potential signaling molecules. Moreover, adipose interlerkin-6 (IL-6) exhibited homologous alterations by obesity and lipolysis. Thus, we postulated a positive feedback loop between ATM and adipocytes via IL-6 signaling backing ATM persistence by comparison of ATM remodeling under obesity and lipolysis. An elucidation of ATM persistence could help to provide novel therapeutic targets for obesity-associated inflammation.
脂肪组织巨噬细胞（ATM）是肥胖症中低度炎症的主要来源，但导致 ATM 在白色脂肪组织（WAT）中积累的原因尚不完全清楚。新出现的证据表明，ATM 在肥胖症中经历了广泛的重塑。除了丰度外，肥胖症中的 ATM 还含有脂质，并进行了代谢重编程，这与它们在肥胖症中的功能改变和持续存在密切相关。在此，我们旨在讨论与 ATM 代谢重编程相关的脂质感应信号的激活对于它们在肥胖症中的迁移、保留或增殖是必不可少的。同样，脂肪分解也诱导了类似但短暂的 ATM 重塑。因此，我们假设肥胖症和脂肪分解在重塑 ATM 方面可能存在重叠的机制。WAT 中冠状结构（CLS）的形成可能是启动 ATM 重塑的常见事件，脂肪细胞释放的一系列脂质代谢物可能是潜在的信号分子。此外，脂肪组织白细胞介素-6（IL-6）通过肥胖症和脂肪分解表现出相似的改变。因此，我们通过比较肥胖症和脂肪分解下的 ATM 重塑，假设 ATM 和脂肪细胞之间通过 IL-6 信号存在正反馈回路，以支持 ATM 的持续存在。阐明 ATM 的持续存在可能有助于为肥胖相关炎症提供新的治疗靶点。
