Key result
Blocking active Fyn-paxillin interaction inhibits vascular smooth muscle cell migration as a potential cardiovascular target.
Review demonstrates how active Fyn-paxillin binding drives vascular smooth muscle cell migration via Rho-kinase, highlighting its potential for treating cardiovascular diseases.
Vascular smooth muscle cell (VSMC) migration plays an important role in cardiovascular diseases, including atherosclerotic plaque formation and restenosis after vascular intervention. The mechanisms involved in VSMC migration are complex and have not been fully elucidated. Recently, we discovered a novel interaction, direct binding of active Fyn-paxillin at focal adhesions, which plays an important role in actin stress fiber formation and migration in VSMCs. In this review, we highlight paxillin as an intermediate signaling molecule that mediates actin stress fiber formation and VSMC migration through the Fyn/paxillin/Rho-kinase signaling pathway by directly binding to active Fyn. We also discuss the inhibition of VSMC migration by blocking the active Fyn-paxillin interaction and the potential of this interaction as a therapeutic target for cardiovascular diseases.
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Zhang et al. (2023) conducted a review in Cardiovascular diseases (atherosclerotic plaque formation and restenosis). Active Fyn-paxillin interaction blockade was evaluated on Vascular smooth muscle cell (VSMC) migration and actin stress fiber formation. Blocking the direct active Fyn-paxillin interaction inhibits vascular smooth muscle cell migration and represents a potential therapeutic target for cardiovascular diseases.
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