{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang Y"],"funding":["HKU State Key Laboratory of Pharmaceutical Biotechnology","HKU","Science and Technology Foundation of Guangdong Province","National Natural Science Foundation of China","Theme-based Research Scheme"],"pagination":["749-763"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5063626"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(4)"],"pubmed_abstract":["Mesenchymal stem cells (MSCs) can donate mitochondria and rescue anthracycline-induced cardiomyocyte (CM) damage, although the underlying mechanisms remain elusive. We determined that the superior efficiency of mitochondrial transfer by human induced-pluripotent-stem-cell-derived MSCs (iPSC-MSCs) compared with bone marrow-derived MSCs (BM-MSCs) is due to high expression of intrinsic Rho GTPase 1 (MIRO1). Further, due to a higher level of TNFαIP2 expression, iPSC-MSCs are more responsive to tumor necrosis factor alpha (TNF-α)-induced tunneling nanotube (TNT) formation for mitochondrial transfer to CMs, which is regulated via the TNF-α/NF-κB/TNFαIP2 signaling pathway. Inhibition of TNFαIP2 or MIRO1 in iPSC-MSCs reduced the efficiency of mitochondrial transfer and decreased CMs protection. Co"],"journal":["Stem cell reports"],"pubmed_title":["iPSC-MSCs with High Intrinsic MIRO1 and Sensitivity to TNF-α Yield Efficacious Mitochondrial Transfer to Rescue Anthracycline-Induced Cardiomyopathy."],"pmcid":["PMC5063626"],"funding_grant_id":["31270967","201007176100","T12-705/11","31571407","201409176221","2015B020225001"],"pubmed_authors":["Chai YH","Tse HF","Chow Y","Liang X","Liang Y","Han S","Li X","Zhang Z","Zhang Y","Xu A","Jiang D","Liao S","Yu Z","Yue W","Lian Q","Chiu SM"],"additional_accession":[]},"is_claimable":false,"name":"iPSC-MSCs with High Intrinsic MIRO1 and Sensitivity to TNF-α Yield Efficacious Mitochondrial Transfer to Rescue Anthracycline-Induced Cardiomyopathy.","description":"Mesenchymal stem cells (MSCs) can donate mitochondria and rescue anthracycline-induced cardiomyocyte (CM) damage, although the underlying mechanisms remain elusive. We determined that the superior efficiency of mitochondrial transfer by human induced-pluripotent-stem-cell-derived MSCs (iPSC-MSCs) compared with bone marrow-derived MSCs (BM-MSCs) is due to high expression of intrinsic Rho GTPase 1 (MIRO1). Further, due to a higher level of TNFαIP2 expression, iPSC-MSCs are more responsive to tumor necrosis factor alpha (TNF-α)-induced tunneling nanotube (TNT) formation for mitochondrial transfer to CMs, which is regulated via the TNF-α/NF-κB/TNFαIP2 signaling pathway. Inhibition of TNFαIP2 or MIRO1 in iPSC-MSCs reduced the efficiency of mitochondrial transfer and decreased CMs protection. Co","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Oct","modification":"2026-05-05T05:44:40.11Z","creation":"2026-04-07T21:30:53.004Z"},"accession":"S-EPMC5063626","cross_references":{"pubmed":["27641650"],"doi":["10.1016/j.stemcr.2016.08.009"]}}