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. 2026 Mar 12:e20936.
doi: 10.1002/advs.202520936. Online ahead of print.

Adhesion-Related Macrophages Regulate Metabolic Homeostasis Through CAV-1 Dependency

Wanyu Hu  1 , Xiyan Liao  2 , Limin Xie  1 , Xiaoxiao Sun  3 , Luodi Jing  1 , Qin Zeng  1 , Hongwei Jiang  3 , Haowei Zhang  4 , Lei Li  5 , Fanqi Wang  1 , Dandan Wang  1 , Ying Mei  1 , Yujin Din  1 , Jianfeng Song  1 , Wufuer Aini  1 , Hui Zhou  1 , Wanqin Xie  6 , Helong Dai  7 , Wei Liu  8 , Joey Liu  9 , Yan Cheng  10   11 , Feng Liu  1 , Willa A Hsueh  9 , Tuo Deng  1
Affiliations

Adhesion-Related Macrophages Regulate Metabolic Homeostasis Through CAV-1 Dependency

Wanyu Hu et al. Adv Sci (Weinh). .

Abstract

The significance of adipose tissue macrophages (ATMs) in regulating adipose tissue function is well-established. However, our investigation revealed a previously overlooked subpopulation of macrophages adhered to adipocytes, which we term adhesion-related macrophages (ARMs). We developed an approach to isolate ARMs and compared them with stromal vascular fraction (SVF) macrophages (SMs). Our findings demonstrate that ARMs constitute the predominant expanded subpopulation of ATMs during obesity, ARMs acquire adipocyte mRNA through direct adhesion to adipocytes, thereby enhancing their lipid processing capacity. Notably, ARMs can be characterized by a key functional marker, Caveolin-1. Genetic ablation of Caveolin-1 in macrophages significantly diminishes ARM abundance, disrupting their adhesion capacity and lipid content, leading to adipocyte hypertrophy, adipose tissue expansion, and impaired glucose homeostasis. Reintroducing ARMs from lean mice into epididymal white adipose tissue (eWAT) mitigates obesity-induced insulin resistance. Our study uncovers ARM as a potential therapeutic target for obesity-induced insulin resistance and opening avenues for identifying similar paradigms in other tissues and diseases.

Keywords: CAV‐1; adipose tissue; insulin resistance; macrophages; obesity.

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References

    1. M. Blüher, “Obesity: Global Epidemiology and Pathogenesis,” Nature reviews Endocrinology 15, no. 5 (2019): 288, https://doi.org/10.1038/s41574‐019‐0176‐8.
    1. G. Ghigliotti, C. Barisione, S. Garibaldi, et al., “Adipose Tissue Immune Response: Novel Triggers and Consequences for Chronic Inflammatory Conditions,” Inflammation 37, no. 4 (2014): 1337–1353, https://doi.org/10.1007/s10753‐014‐9914‐1.
    1. S. Cinti, G. Mitchell, G. Barbatelli, et al., “Adipocyte Death Defines Macrophage Localization and Function in Adipose Tissue of Obese Mice and Humans,” Journal of Lipid Research 46, no. 11 (2005): 2347–2355, https://doi.org/10.1194/jlr.M500294‐JLR200.
    1. S. Cao, Y. Pan, J. Tang, et al., “EGFR‐Mediated Activation of Adipose Tissue Macrophages Promotes Obesity and Insulin Resistance,” Nature Communications 13, no. 1 (2022): 4684, https://doi.org/10.1038/s41467‐022‐32348‐3.
    1. G. Fantuzzi, “Adipose Tissue, Adipokines, and Inflammation,” Journal of Allergy and Clinical Immunology 115, no. 5 (2005): 911–919, https://doi.org/10.1016/j.jaci.2005.02.023.