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Life sciences · Journal article
Metabolism and Target Organ Damage · October 8, 2026
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Obesity is a systemic driver of cellular dysfunction that reshapes tissue biology well beyond energy storage, extending its influence to the regenerative machinery of the body. Mesenchymal stem/stromal cells (MSCs) support tissue repair through immunomodulatory, angiogenic, and paracrine functions, and accumulating evidence indicates that obesity impairs these functions within its metabolic milieu. This review integrates the mitochondrial, epigenetic, epitranscriptomic, and extracellular vesicle (EV) mechanisms by which obesity reprograms MSCs, traces the functional and organ-level consequences, and appraises rescue strategies against the strength and translational maturity of the supporting evidence. In the nutrient-excess environment of obesity, lipotoxicity, oxidative stress, and low-grade inflammation converge to erode mitochondrial integrity and bioenergetic homeostasis. Mitochondrial dysfunction is reinforced by dysregulated adenosine monophosphate-activated protein kinase (AMPK)-mechanistic target of rapamycin (mTOR) signaling, defective autophagy and mitophagy, and perturbed nicotinamide adenine dinucleotide (NAD+)-sirtuin homeostasis. These abnormalities intersect with epigenetic and epitranscriptomic remodeling, including altered chromatin regulation and non-coding ribonucleic acid signaling, as well as changes in EV cargo. Collectively, these interconnected processes reduce MSC stemness and metabolic adaptability, promote senescence and inflammatory phenotypes, and compromise reparative function. Consequently, obesity-compromised MSCs exhibit diminished immunomodulatory, angiogenic, and regenerative potential, which may limit their protective function across organs such as the heart, liver, and kidney and constrain their use as an autologous therapeutic. We discuss evolving therapeutic strategies, including metabolic reprogramming, mitochondrial protection, NAD+ restoration, senolytic approaches, and MSC- or EV-based interventions, and outline the translational gaps that remain before these approaches can benefit metabolically compromised patients.