ArticleActa pharmaceutica Sinica. B2024
Adiponectin restores the obesity-induced impaired immunomodulatory function of mesenchymal stromal cells
Article in Acta pharmaceutica Sinica. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Leptin sensitizes hepatocytes to endotoxin toxicity via interleukin-1β signaling and drives adaptive immune activation in the liver.Archives of pharmacal research · 2026Article
- Gnetum Montanum Markgr. Extract mitigates gouty arthritis by targeting urate crystal-induced NLRP3 inflammasome activation.Journal of natural medicines · 2026Article
- SUMOylation is a Translatable Target in Hypoxic MNPs Regulating Retinal Vasculopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Challenges and opportunities in obesity: the role of adipocytes during tissue fibrosis.Frontiers in endocrinology · 2024Review
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Authors and funding
7 authors.
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Abstract
Obesity has been known to negatively modulate the life-span and immunosuppressive potential of mesenchymal stromal cells (MSC). However, it remains unclear what drives the compromised potency of obese MSC. In this study, we examined the involvement of adiponectin, an adipose tissue-derived hormone, in obesity-induced impaired therapeutic function of MSC. Diet-induced obesity leads to a decrease in serum adiponectin, accompanied by impairment of survival and immunomodulatory effects of adipose-derived MSC (ADSC). Interestingly, priming with globular adiponectin (gAcrp) improved the immunomodulatory potential of obese ADSC. Similar effects were also observed in lean ADSC. In addition, gAcrp potentiated the therapeutic effectiveness of ADSC in a mouse model of DSS-induced colitis. Mechanistically, while obesity inhibited the glycolytic capacity of MSC, gAcrp treatment induced a metabolic shift toward glycolysis through activation of adiponectin receptor type 1/p38 MAPK/hypoxia inducible factor-1
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