{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cho HJ"],"funding":["National Research Foundation of Korea"],"pagination":["760"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9440251"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(9)"],"pubmed_abstract":["Selective removal of senescent cells, or senolytic therapy, has been proposed to be a potent strategy for overcoming age-related diseases and even for reversing aging. We found that nintedanib, a tyrosine kinase inhibitor, selectively induced the death of primary human dermal fibroblasts undergoing RS. Similar to ABT263, a well-known senolytic agent, nintedanib triggered intrinsic apoptosis in senescent cells. Additionally, at the concentration producing the senolytic effect, nintedanib arrested the cell cycle of nonsenescent cells in the G1 phase without inducing cytotoxicity. Interestingly, the mechanism by which nintedanib activated caspase-9 in the intrinsic apoptotic pathway differed from that of ABT263 apoptosis induction; specifically, nintedanib did not decrease the levels of Bcl-2"],"journal":["Cell death & disease"],"pubmed_title":["Nintedanib induces senolytic effect via STAT3 inhibition."],"pmcid":["PMC9440251"],"funding_grant_id":["2022R1I1A1A01066031","2021R1A2C1008983","2015R1A5A2009124","2020M3A9D8038014","2020R1A2C2013416"],"pubmed_authors":["Lee YS","Hwang JA","Kim SY","Park SC","Kim YZ","Cho HJ","Yang EJ","Kim EC","Kim JR"],"additional_accession":[]},"is_claimable":false,"name":"Nintedanib induces senolytic effect via STAT3 inhibition.","description":"Selective removal of senescent cells, or senolytic therapy, has been proposed to be a potent strategy for overcoming age-related diseases and even for reversing aging. We found that nintedanib, a tyrosine kinase inhibitor, selectively induced the death of primary human dermal fibroblasts undergoing RS. Similar to ABT263, a well-known senolytic agent, nintedanib triggered intrinsic apoptosis in senescent cells. Additionally, at the concentration producing the senolytic effect, nintedanib arrested the cell cycle of nonsenescent cells in the G1 phase without inducing cytotoxicity. Interestingly, the mechanism by which nintedanib activated caspase-9 in the intrinsic apoptotic pathway differed from that of ABT263 apoptosis induction; specifically, nintedanib did not decrease the levels of Bcl-2","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2026-05-10T05:13:51.787Z","creation":"2025-02-19T04:03:12.935Z"},"accession":"S-EPMC9440251","cross_references":{"pubmed":["36055997"],"doi":["10.1038/s41419-022-05207-8"]}}