{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang Q"],"funding":["Natural Science Foundation of Beijing Municipality","Australian Research Council Future Fellow","MOST | National Natural Science Foundation of China (NSFC)","The Taishan Scholar Project of Shandong Province of China","National Natural Science Foundation of China","China Postdoctoral Science Foundation","Key Technology Research and Development Program of Shandong Province","Key Research and Development Program of Shandong Province","China Postdoctoral Science Foundation (China Postdoctoral Foundation Project)","Beijing Natural Science Foundation"],"pagination":["e71020"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12413656"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(17)"],"pubmed_abstract":["Restenosis following endovascular intervention in lower extremity arterial disease contributes to significant morbidity and mortality. This study investigates the role of formylpeptide receptor 2 (FPR2) in neointimal hyperplasia and evaluates the therapeutic potential of the selective FPR2 agonist BMS-986235 in mitigating restenosis. FPR2 expression was significantly reduced in the popliteal and anterior tibial arteries of male amputees with restenosis compared to healthy controls. Whole-body and myeloid-specific FPR2 knockout mice consistently displayed exaggerated neointimal hyperplasia, accompanied by a marked reduction in vessel lumen diameter, following endothelial injury. Treatment with BMS-986235 effectively slowed the progression of restenosis. Mechanistically, FPR2 activation main"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6."],"pmcid":["PMC12413656"],"funding_grant_id":["FT250100365","no.tsqn202408367","82073840","82100891","No.7254372","81800732","2021M691957","82270888","no.tsqn201812016","2021ZLGX02"],"pubmed_authors":["Zhou M","Zhao P","Zha Y","Chen Y","Wang X","Woodman OL","Zhou X","Qin CX","Zhang Q"],"additional_accession":[]},"is_claimable":false,"name":"FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6.","description":"Restenosis following endovascular intervention in lower extremity arterial disease contributes to significant morbidity and mortality. This study investigates the role of formylpeptide receptor 2 (FPR2) in neointimal hyperplasia and evaluates the therapeutic potential of the selective FPR2 agonist BMS-986235 in mitigating restenosis. FPR2 expression was significantly reduced in the popliteal and anterior tibial arteries of male amputees with restenosis compared to healthy controls. Whole-body and myeloid-specific FPR2 knockout mice consistently displayed exaggerated neointimal hyperplasia, accompanied by a marked reduction in vessel lumen diameter, following endothelial injury. Treatment with BMS-986235 effectively slowed the progression of restenosis. Mechanistically, FPR2 activation main","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-02T22:34:49.436Z","creation":"2026-05-28T03:06:38.976Z"},"accession":"S-EPMC12413656","cross_references":{"pubmed":["40913417"],"doi":["10.1096/fj.202501823R"]}}