Increased cellular senescence in the murine and human stenotic kidney: Effect of mesenchymal stem cells

摘要: Cell stress may give rise to insuperable growth arrest, which is defined as cellular senescence. Stenotic kidney (STK) ischemia and injury induced by renal artery stenosis (RAS) be associated with Mesenchymal stem cells (MSCs) decrease some forms of STK injury, but their ability reverse senescence in RAS remains unknown. We hypothesized that evokes senescence, would ameliorated MSCs. Mice were studied after 4 weeks RAS, treated adipose tissue-derived MSCs 2 earlier, or sham. senescence-associated β-galactosidase (SA-β-Gal) activity was measured. Protein gene expression used assess the secretory phenotype (SASP), staining for fibrosis, inflammation, capillary density. In addition, assessed p16+ p21+ urinary exosomes patients renovascular hypertension (RVH) without 3 months autologous MSC delivery, healthy volunteers (HV). mice, SA-β-Gal increased, SASP marker markedly elevated. improved function, density, attenuated activity, most levels remained unchanged. Congruently, human RVH, elevated compared HV, only slightly MSC, whereas Therefore, triggers both mice subjects. partly mitigate These observations support exploration targeted senolytic therapy RAS.