ArticleStem cell research & therapy2025
MSCs-derived HGF alleviates senescence after AKI by modulating mitoSTAT3-controlled copper flux and respiration.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Overexpression of Soluble Fibrinogen-like Protein 2 in MSCs Ameliorates Renal Ischemia-Reperfusion Injury in Mice by Modulating Neutrophils.Balkan medical journal · 2026Article
- p53-associated regulation of COX17 enhances elesclomol-induced copper-associated cytotoxicity and suppresses gastric cancer growth.Frontiers in immunology · 2026Article
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Authors and funding
11 authors.
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Abstract
backgroundHuman umbilical cord-derived mesenchymal stem cells (hUC-MSCs) can reverse senescence after acute kidney injury (AKI) via maintaining mitochondrial homeostasis. Copper accumulation and STAT3 nuclear translocation promote senescence, but their mitochondrial localization in response to MSCs remains unclear.
methodsC57 mice with renal unilateral ischemia reperfusion injury (uIRI) were renal capsular transplanted with hUC-MSCs for two weeks to assessed treatment efficacy. Then, RNA sequencing, protein co-immunoprecipitation, molecular docking, and molecular dynamic simulation were used to found the relationship between senescence, mitochondrial translocation of STAT3 (mitoSTAT3), and copper homeostasis. Furthermore, inhibition of cMet/HGFR, mitoSTAT3, or COX17 were used to validated their contact.
resultsHUC-MSCs improved renal function, reduced senescence markers (SA-β-gal, p53, p21, p16), and increased STAT3pSer727 and COX17 levels. RNA sequencing revealed that senescence regulation is associated with copper homeostasis and respiratory chain complex IV. Blocking MSCs-derived HGF via lentivirus decreased STAT3pSer727, COX17, and mt-Co1 (a key subunit of complex IV). Co-immunoprecipitation and molecular docking confirmed tight binding between STAT3pSer727 and COX17. Inhibiting cMet produced similar effects as HGF deficiency, with increasing mitochondrial copper and decreasing mt-Co1. In hypoxic renal tubular epithelial cells (RTECs), blocking HGF or cMet diminished STAT3 mitochondrial translocation, and inhibiting mitoSTAT3 decreased COX17 and mt-Co1. Furthermore, knockdown COX17 aggravated loss of complex IV activity, copper accumulation and RTECs senescence.
conclusionsHUC-MSCs-derived HGF promotes STAT3 mitochondrial translocation via cMet, enhancing mitochondrial respiration and copper excretion through COX17, thereby reducing renal senescence after AKI.
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