Demonstrates enhanced vascular integrity in cardiovascular implants, suggesting improved biocompatibility.
Cardiovascular implants are often limited by adverse interactions between synthetic surfaces and blood components, which hinder re-endothelialization and induce abnormal healing responses that lead to late restenosis. Adequate luminal protection requires a continuous, autologous endothelial layer that restores vascular health. Here, we present a surface modification strategy using macrophage-derived membrane vesicles functionalized with ligands targeting inflamed endothelial cell receptors. This biomimetic coating promotes ligand-receptor interactions at the implant interface, thereby accelerating endothelialization. Notably, the coated surface supports the coexistence of endothelial cells and vascular smooth muscle cells (vSMCs), suppressing their inflammatory transition to a synthetic phenotype. The vesicle-coated interface stabilizes endothelial monolayers by reducing NF-κB activation and regulating von Willebrand factor (vWF), ultimately maintaining VE-cadherin-mediated junction integrity under inflammatory conditions. This approach offers a clinically relevant strategy for enhancing the biocompatibility and functional integration of cardiovascular implants, warranting further validation on medical-grade metals and in vivo models.
No takes yet. Share an insight, caveat, or question.
Hasan et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: