{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhuang K"],"funding":["Natural Science Foundation of Beijing Municipality","National Natural Science Foundation of China","China Postdoctoral Science Foundation"],"pagination":["526"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12482249"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["<h4>Background</h4>Human 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.<h4>Methods</h4>C57 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 u"],"journal":["Stem cell research & therapy"],"pubmed_title":["MSCs-derived HGF alleviates senescence after AKI by modulating mitoSTAT3-controlled copper flux and respiration."],"pmcid":["PMC12482249"],"funding_grant_id":["82170686","2024M754288","7254312","No. 82200762"],"pubmed_authors":["Zheng X","Feng Z","Wang S","Zhang Y","Liang Y","Xu C","Wang W","Chen Y","Chen X","Zhuang K","Cai G"],"additional_accession":[]},"is_claimable":false,"name":"MSCs-derived HGF alleviates senescence after AKI by modulating mitoSTAT3-controlled copper flux and respiration.","description":"<h4>Background</h4>Human 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.<h4>Methods</h4>C57 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 u","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-07-15T09:49:53.62Z","creation":"2026-07-02T03:12:13.417Z"},"accession":"S-EPMC12482249","cross_references":{"pubmed":["41024282"],"doi":["10.1186/s13287-025-04653-3"]}}