biostudies-literatureZhang QNatural Science Foundation of Beijing MunicipalityAustralian Research Council Future FellowMOST | National Natural Science Foundation of China (NSFC)The Taishan Scholar Project of Shandong Province of ChinaNational Natural Science Foundation of ChinaChina Postdoctoral Science FoundationKey Technology Research and Development Program of Shandong ProvinceKey Research and Development Program of Shandong ProvinceChina Postdoctoral Science Foundation (China Postdoctoral Foundation Project)Beijing Natural Science Foundatione71020https://www.ebi.ac.uk/biostudies/studies/S-EPMC12413656biostudies-literatureUnknown39(17)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 mainFASEB journal : official publication of the Federation of American Societies for Experimental BiologyFPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6.PMC12413656FT250100365no.tsqn2024083678207384082100891No.7254372818007322021M69195782270888no.tsqn2018120162021ZLGX02Zhou MZhao PZha YChen YWang XWoodman OLZhou XQin CXZhang QfalseFPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6.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 main2025-01-01T00:00:00Z2025 Sep2026-06-02T22:34:49.436Z2026-05-28T03:06:38.976ZS-EPMC124136564091341710.1096/fj.202501823R