March 3, 2026Open Access

Vascular smooth muscle cell RNA-binding protein U2AF2 induces copper death by regulating C1qbp expression, delaying development of atherosclerosise

Key Points

Induction of copper death alters atherosclerosis development, affecting vascular smooth muscle cells directly and through the U2AF2-C1qbp axis.
Targeted inhibition of U2AF2 may delay lesions related to atherosclerosis, providing a new therapeutic angle with implications for treatment.
Analysis highlights the regulatory relationship between U2AF2 and C1qbp, contributing to significant pathways in atherosclerosis development.
Copper death mechanisms offer novel insight into the treatment of atherosclerosis, with potential wider applications in vascular health.

Abstract

This study revealed the role of the U2AF2-C1qbp-copper death regulatory axis in the development of AS, providing new targets and a theoretical basis for the treatment of AS. Targeted inhibition of U2AF2 may become an effective strategy to delay progression of AS.

Vascular smooth muscle cell RNA-binding protein U2AF2 induces copper death by regulating C1qbp expression, delaying development of atherosclerosise

Key Points

Abstract

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