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. 2023 Feb 7;55(2):313–324. doi: 10.1038/s12276-023-00940-2

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Obesity induces an imbalance in the production and secretion of adipokines. Some adipokines, such adiponectin and omentin-1, are downregulated, whereas most of others are upregulated in response to excess adiposity. High levels of leptin, visfatin, and resistin in the MSC niche promote the differentiation of MSC to adipocytes, impaired pleiotropic functions, and accelerate senescence and apoptotic cell death. In addition, downregulation of adiponectin and omentin-1, which play a critical role in the maintenance of survival and functional plasticity of MSC, further contributes to impaired MSC functions. Consequently, obese-derived MSC has exhibited the lower efficacy in treatment of various disorders. Given the role of MSC as critical regulators of inflammatory and immune responses, adipogenesis, and tissue repair and regeneration, abnormal function of MSC in obese subjects would exacerbate adipose tissue (AT) inflammation and remodeling, as well as promote the initiation and progression of obesity-associated complications.