The Transfer of USP25 by Exosomes of Adipose Tissue-Derived Mesenchymal Stem Cells Ameliorates Diabetic Nephropathy Through Stabilizing SMAD7 Expression.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Adipose tissue-derived mesenchymal stem cells (ADSCs) are identified to be potential therapeutic candidates for diabetic nephropathy (DN) through secreting exosomes (Exos). Ubiquitin-specific protease 25 (USP25) has been reported to be involved in DN-induced renal injury. Herein, this study aimed to investigate whether ADSCs affected DN progression by Exo transfer of USP25. High glucose (HG)-induced mouse podocytes were used to mimic DN-induced injury for in vitro viability, inflammation, and apoptosis analyses. The db/db mice of DN were established for renal injury and function analysis in vivo. The deubiquitination effect of USP25 was analyzed by cellular ubiquitination and immunoprecipitation assays. ADSCs reversed HG-induced apoptosis and inflammation in podocytes, and these effects were achieved by Exo-mediated transfer of USP25. Mechanistically, USP25 interacted with SMAD7 protein and elevated its expression in podocytes via inducing SMAD7 deubiquitination. USP25 transferred via ADSC-Exos abolished HG-induced apoptosis and inflammation in podocytes by elevating SMAD7 protein levels. In vivo assay also confirmed that ADSC-Exo attenuated Type 2 Diabetes Mellitus-induced kidney injury and podocyte apoptosis and inflammation by releasing USP25. ADSCs attenuated T2DM-induced kidney injury, podocyte apoptosis, and inflammation via elevating SMAD7 stabilization through exosome t

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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