Fibroblast activation protein mediates vascular restenosis after surgery for peripheral arterial disease

Fibroblast activation protein mediates vascular restenosis after surgery for peripheral arterial disease. Fibroblast activation protein mediates vascular restenosis after surgery for peripheral arterial disease Article Open access Published: 30 October 2026 Cite this article You have full access to this open access article Download PDF View saved research Fibroblast activation protein mediates vascular restenosis after surgery for peripheral arterial disease Download PDF Abstract Postoperative vascular restenosis hampers long-term surgical outcomes in peripheral arterial disease (PAD). Aberrant vascular smooth muscle cell (VSMC) migration and proliferation drive neointimal hyperplasia, the core pathological feature of restenosis, yet key molecular regulators remain incompletely defined.

This study characterizes fibroblast activation protein (FAP): GEO bioinformatics analyses nominated FAP as a candidate regulator. FAP is low in normal arteries but markedly upregulated in injured vessels and synthetic-phenotype VSMCs, correlating positively with VSMC migration. FAP knockdown represses VSMC migration in vitro and attenuates neointimal hyperplasia in vivo.

RNA-sequencing implicates FAP in modulating the Net1–RhoA–ROCK axis, further validated by western blot. Collectively, FAP upregulation promotes VSMC migration to foster neointimal hyperplasia and restenosis, marking FAP as a potential biomarker and therapeutic target for PAD-associated restenosis. Explore related subjects Discover the latest articles and news in related subjects.

Medical Disclaimer: This article is for informational purposes only and does not constitute medical advice. Always consult with qualified healthcare professionals for medical decisions and treatment options.