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Updated: Dec 15, 2025
Prospective, Randomized, and Controlled Study of a Human Umbilical Cord Mesenchymal Stem Cell Injection for Treating Diabetic Foot Ulcers
Published on: March 3, 2023
Human umbilical cord mesenchymal stem cell attenuates renal fibrosis via TGF-β/Smad signaling pathways in vivo and in
Yihang Yu1, Dong Hu1, Yu Zhou1
1Department of Urology, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China; Chongqing Key Laboratory of Children Urogenital Department and Tissue Engineering, Chongqing, 400014, China; Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, 400014, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing, 400014, China; National Clinical Research Center for Child Health and Disorders, Chongqing, 400014, China; Chongqing Key Laboratory of Pediatrics, Chongqing, 400014, China.
Abstract:
Renal fibrosis is a progressive pathological process that eventually leads to end-stage renal failure with limited therapeutic options. The aim of this study was to investigate the nephron-protective effect of human umbilical cord mesenchymal stem cells (ucMSCs) on renal fibrosis. UcMSCs were intravenously injected into renal fibrosis mice induced by aristolochic acid (AA) and co-cultured with HK-2 cells induced by TGF-β1, respectively. The kidney functions including serum creatinine (Scr) and blood urea nitrogen (BUN) levels, and histopathology were examined after treated with stem cells and normal saline as control. Immunohistochemical staining, immunofluorescent staining, and Western blot analysis were used to assessed the expression of proteins associated with epithelial to mesenchymal transition (EMT) and TGF-β/Smad signaling pathway. The results showed that ucMSCs effectively improved the kidney function and pathological structure, reduced AA-induced fibrosis and extracellular matrix deposition. Besides, UcMSCs significantly inhibited the EMT process and TGF-β1/Smad signaling pathway in AA-induced mice and TGF-β1-induced HK-2 cells compared to the control (p < 0.05). Our data suggested that ucMSCs play as a nephron-protective role in anti-fibrosis through inhibiting the activation of TGF-β1/Smad signaling pathway.
