ArticleAtherosclerosis plus2025
Earthworm fibrinolytic enzyme A and fibrin-derived peptide Bβ15-42 attenuate atherosclerosis via the VE-Cadherin signaling pathway.
Article in Atherosclerosis plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aim: Earthworm fibrinolytic enzymes A (EFEa) is the main active component of earthworm fibrinolytic enzymes which possesses anticoagulant, fibrinolytic, and potential anti-atherosclerotic effects. However, the biological function and mechanism of action of EFEa remains unclear. This study aims to investigate the role of EFEa and the fibrin-derived peptide Bβ15-42 (Bβ15-42) in attenuating atherosclerosis by modulating endothelial adhesion and inflammation via the vascular endothelial (VE)-cadherin signaling pathway. Methods: In this study, we established both a rabbit model of atherosclerosis and an in vitro endothelial cell model. Bβ15-42, EFEa, and rosuvastatin (ROS) were administered to evaluate their effects on atherosclerotic plaque formation and inflammatory responses. Plaque size and intimal thickening were evaluated using Oil Red O and hematoxylin-eosin (HE) staining. Fibrinogen deposition and VE-cadherin expression were analyzed via western blotting and immunohistochemistry. Furthermore, macrophage migration assays and CDH5-positive (CDH5 Results: Treatment with Bβ15-42, EFEa, and ROS significantly reduced atherosclerotic plaque formation and intimal thickening in the rabbit model of atherosclerosis ( Conclusion: EFEa and Bβ15-42 exert protective effects against atherosclerosis via the VE-cadherin pathway. Our findings lay the groundwork for further research into the anti-atherosclerotic mechanisms of EFEa, as well as its potential for future development and application.
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