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Bif-1 induces vascular remodeling in injured rat carotid artery by engaging β-catenin signaling.

Jie Wei,Chaorui Wang,Jie Li,Yi Xu,Xin Jiang,Han Wei,Ning Hou,Yun Liu

Published 2025 in The Journal of pharmacy and pharmacology

ABSTRACT

BACKGROUND Bax-interacting factor-1 (Bif-1) is well-documented in the regulation of cancers and neurodegenerative disorders. However, its role in vascular diseases remains largely unexplored. Here, we demonstrate a critical role for Bif-1 in the pathogenesis of vascular remodeling following injury. METHODS AND RESULTS Using both knockdown and overexpression strategies, we found that Bif-1 knockdown inhibited the proliferation, migration, and phenotypic switch of vascular smooth muscle cells (VSMCs) and attenuated vascular remodeling upon injury. Conversely, Bif-1 overexpression exacerbated these pathological processes. Mechanistically, we showed that β-catenin signaling was regulated by Bif-1. Importantly, the interaction between Bif-1 and Axin2 was promoted upon angiotensin II (Ang II) stimulation, which is correlated with the activation of β-catenin signaling. CONCLUSIONS Together, our findings suggest that Bif-1 is a novel vascular injury-response molecule that promotes VSMC proliferation, migration, and phenotypic switch. Thus, the inhibition of Bif-1-mediated activation of β-catenin signaling represents a promising therapeutic strategy for preventing VSMC accumulation and vascular obstructive diseases following injury.

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