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An emerging role for eosinophils as pro-angiogenic drivers of adipose tissue beiging

脂肪组织 血管生成 生物 脂肪组织巨噬细胞 产热 细胞生物学 免疫系统 白色脂肪组织 脂肪因子 内科学 内分泌学 褐色脂肪组织 新生血管 炎症 组织重塑 功能(生物学) 再生医学 免疫学 组织工程
作者
Tia J. Valentini,Annalise M. Spek,Kate Quinlan
出处
期刊:Clinical Science [Portland Press]
卷期号:140 (5): 663-679
标识
DOI:10.1042/cs20250051
摘要

Adipose tissue is a metabolically dynamic organ that undergoes extensive remodelling to maintain homeostasis. Beige adipose tissue is an inducible type of thermogenic fat that releases stored energy as heat and is therefore an attractive target for an anti-obesity therapy that drives weight loss through an increase in energy expenditure. Adipose tissue must undergo remodelling during the process of beiging, including increasing vascularisation via angiogenesis. Angiogenesis itself is also a potential target for a pro-beiging therapy, as it can promote beiging. Immune cells are essential in the adipose tissue to support thermogenesis; however, the potential involvement of immune cells in the regulation of adipose tissue angiogenesis is not well understood. Adipose-resident eosinophils in particular have emerged as key drivers of beiging. Notably, eosinophils exhibit pro-angiogenic activity in other tissues; however, a possible pro-angiogenic function of eosinophils in the adipose tissue specifically has not been explored. The present review summarises our current knowledge of adipose tissue remodelling during tissue expansion in the development of obesity and during beiging. We present the evidence for the link between angiogenesis and thermogenesis and synthesise the established role of eosinophils in beiging and in angiogenesis in other tissue contexts to propose a hypothesis: eosinophils may promote beiging indirectly in the adipose tissue by driving angiogenesis. We further evaluate the therapeutic potential of targeting angiogenesis in the treatment of obesity. Understanding the processes that drive healthy remodelling of the tissue during beiging could reveal new avenues for anti-obesity pharmacotherapies that increase energy expenditure via pro-beiging mechanisms.
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