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Vascular smooth muscle cell (VSMC) proliferation and neointima formation play significant roles in atherosclerosis development and restenosis following percutaneous coronary intervention. Our team previously discovered that TEA domain transcription factor 1 (TEAD1) promotes vascular smooth muscle differentiation, which is necessary for vascular development. Conversely, aberrant YAP1 activation upregulates the platelet-derived growth factor receptor beta to encourage VSMC proliferation and neointima formation. In this study, we aimed to investigate the molecular mechanisms of YAP1/TEAD signaling during neointima formation. Our research focused on the prolyl 4-hydroxylase alpha 2 (P4HA2) and its downstream target, Yes-associated protein 1 (YAP1), in regulating VSMC differentiation and neointima formation. Our results indicated that P4HA2 reduction leads to VSMC dedifferentiation and promotes neointima formation after injury. Furthermore, we found that P4HA2-induced prolyl hydroxylation of YAP1 restricts its transcriptional activity, which is essential to maintaining VSMC differentiation. These findings suggest that targeting P4HA2-mediated prolyl hydroxylation of YAP1 may be a promising therapeutic approach to prevent injury-induced neointima formation in cardiovascular disease. Copyright © 2023 Elsevier Inc. All rights reserved.


Liang Wang, Ting Liu, Yaofu Zheng, Jiamin Zhou, Hexiang Hua, Liming Kong, Weilin Huang, Xiaoping Peng, Tong Wen. P4HA2-induced prolyl hydroxylation of YAP1 restricts vascular smooth muscle cell proliferation and neointima formation. Life sciences. 2023 Oct 01;330:122002

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PMID: 37549826

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