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. 2022 Aug 25;13:935275. doi: 10.3389/fimmu.2022.935275

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Copyright © 2022 Xiong, Tan, Wang, He, Hu, Wu, Liu, Lin, Li, Chen and Mao

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Cellular and molecular mechanisms of adipose tissue fibrosis. Myofibroblasts are pivotal for ECM production and remodeling. Adipocyte progenitors can differentiate into myofibroblasts, which then drive ECM synthesis. Adipocyte progenitors express both PDGFRα and PDGFRβ. When PDGFRα signaling is activated, adipocyte progenitors synthesize ECM and function as profibrotic cells. PDGFRβ inhibits the adipogenic potential of progenitors. The nuclear receptor PPARγ also regulates adipogenesis with anti-fibrotic potential. Moreover, TGF-β1, activin A, CTGF, GH, and MRTFA may drive adipose progenitors to acquire a myofibroblast phenotype and prevent differentiation into adipocytes under certain circumstances. The infiltrating macrophages in adipose tissue can release signals, such as IL-6, MCP-1, TNF-α, and IL-1β, which attract fibroblasts and regulate adipose tissue fibrosis. In addition, macrophage-inducible C-type lectin (Mincle) modulates macrophage function and correlates with myofibroblast activation and ECM remodeling. Mast cells secrete MCP-6 and induce collagen V expression, contributing to adipose tissue fibrosis and accelerating insulin resistance by inhibiting preadipocyte differentiation. ILC1 in adipose tissue induces fat fibrosis in an IFN-γ-dependent manner. HIF1α promotes adipose tissue fibrosis and is a potential therapeutic target for adipose tissue fibrosis and associated metabolic disorders. ECM, extracellular matrix; PDGF, platelet-derived growth factor; PPARγ, peroxisome proliferator-activated receptor-gamma; TGF-β1, transforming growth factor-beta 1; CTGF, connective tissue growth factor; GH, growth hormone; MRTFA, myocardin-related transcription factor A; IL-6, interleukin-6; MCP-1, monocyte chemoattractant protein-1; TNF-α, tumor necrosis factor-alpha; IL-1β: interleukin-1beta; MCP-6, mast cell protease 6; ILC1s, group 1 innate lymphoid cells; IFN-γ, interferon-gamma; HIF1α, hypoxia-inducible factor 1-alpha.