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Abstract: TH-PO648

Impact of Obesity on Mesenchymal Stem Cell Senescence

Session Information

Category: Development, Stem Cells, and Regenerative Medicine

  • 501 Development, Stem Cells, and Regenerative Medicine: Basic


  • Conley, Sabena, Mayo Clinic, Rochester, Minnesota, United States
  • Kim, Seo Rin, Mayo Clinic , Rochester, Minnesota, United States
  • Tang, Hui, Mayo Clinic, Rochester, Minnesota, United States
  • Zhu, Xiang yang, Mayo Clinic, Rochester, Minnesota, United States
  • Kirkland, James L., Mayo Clinic, Rochester, Minnesota, United States
  • Hickson, LaTonya J., Mayo Clinic, Rochester, Minnesota, United States
  • Lerman, Lilach O., Mayo Clinic College of Medicine, Rochester, Minnesota, United States

Obesity induces inflammation and contributes to the pathogenesis of kidney disease. Endogenous mesenchymal stem/stromal cells (MSC) mediate tissue repair, and show promise as exogenous therapy of kidney injury. However, chronic inflammation may impair the regenerative potential of MSC. We hypothesized that in human adipose tissue-derived MSC, obesity induces senescence, a growth-arrest program that transitions cells to a pro-inflammatory state.


MSC proliferation and migration were studied in MSC harvested from subcutaneous abdominal fat from obese (n=6, BMI ≥35 kg/m2) and age-matched lean controls (n=6, BMI <30 kg/m2) during bariatric or kidney donation surgeries. Cellular senescence was evaluated by senescence-associated β-galactosidase (SA-β-gal) activity (staining), and by expression of cell cycle arrest (p21) and senescent-associated secretory phenotype (SASP) (MCP-1, IL-1α, and PAI-1) markers (quantitative PCR).


Among all subjects, mean age was 59±8 years, eGFR 64.8±15.3 mL/min/1.73m2, and 66% were females. Obese-MSC exhibited similar proliferation capacity as Control-MSC, but their migratory potential was lower, suggesting MSC dysfunction (Fig A). Senescence burden as per SA-β-gal staining, p21 and SASP markers expression was elevated in Obese-MSC (Figs B-C).


Human obesity induces senescence in adipose tissue-derived MSC. This impairment in endogenous cellular repair systems may permit development of kidney lesions that are inadequately repaired in subjects with obesity, and limit delivery of autologous MSC to the subjects kidneys'.


  • NIDDK Support