FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6.

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

SUBMITTER: Zhang Q 

PROVIDER: S-EPMC12413656 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature