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Lipedema: A Disease Triggered by M2 Polarized Macrophages?

ORCID
0000-0002-7937-8887
Affiliation
School of Pharmacy, Faculty of Medicine and Health, University of Sydney, Sydney, NSW 2006, Australia;
Grewal, Thomas;
Affiliation
Department of Plastic, Hand, and Reconstructive Surgery, University Hospital Regensburg, 93053 Regensburg, Germany;
Kempa, Sally;
ORCID
0000-0002-5635-3994
Affiliation
Department of Internal Medicine I, University Hospital Regensburg, 93053 Regensburg, Germany
Buechler, Christa

Background/Objectives : Lipedema is a progressive disease that results in the bilateral and symmetrical accumulation of subcutaneous fat in the legs and/or arms, affecting almost exclusively women. Methods : A comprehensive review of the peer-reviewed literature was conducted between November 2024 and February 2025. Results : The pathophysiology of lipedema is complex and, especially in the early stages, shows similarities to obesity, involving adipocytes, adipose tissue-resident macrophages, and endothelial cells. In lipedema, systemic levels and the adipocyte expression of the classical adipokines adiponectin and leptin appear normal, while it remains unclear if markers of inflammation and oxidative stress are increased. Macrophages in the adipose tissue of patients have an anti-inflammatory M2 phenotype and express high levels of the scavenger receptor CD163. These cells affect adipogenesis and seem to have a central role in adipose tissue accumulation. Increased lymphatic and blood vessel permeability are comorbidities of lipedema that occur in early disease states and may contribute to disease progression. Conclusions : This review summarizes our current understanding of the pathophysiology of lipedema with a focus on the role of stromal vascular localized M2 macrophages.

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License Holder: © 2025 by the authors.

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