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Acetate controls endothelial-to-mesenchymal transition
Journal article   Peer reviewed

Acetate controls endothelial-to-mesenchymal transition

Xiaolong Zhu, Yunyun Wang, Ioana Soaita, Heon-Woo Lee, Hosung Bae, Nabil Boutagy, Anna Bostwick, Rong-Mo Zhang, Caitlyn Bowman, Yanying Xu, …
Cell metabolism, Vol.35(7), pp.1163-1178.e10
07/11/2023
DOI: 10.1016/j.cmet.2023.05.010
PMID: 37327791

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Abstract

Endothelial-to-mesenchymal transition (EndMT), a process initiated by activation of endothelial TGF-(3 signaling, underlies numerous chronic vascular diseases and fibrotic states. Once induced, EndMT leads to a further increase in TGF-(3 signaling, thus establishing a positive-feedback loop with EndMT leading to more EndMT. Although EndMT is understood at the cellular level, the molecular basis of TGF-(3-driven EndMT induction and persistence remains largely unknown. Here, we show that metabolic modulation of the endothelium, triggered by atypical production of acetate from glucose, underlies TGF-(3-driven EndMT. Induction of EndMT suppresses the expression of the enzyme PDK4, which leads to an increase in ACSS2-dependent Ac-CoA synthesis from pyruvate-derived acetate. This increased Ac-CoA production results in acetylation of the TGF-(3 receptor ALK5 and SMADs 2 and 4 leading to activation and long-term stabilization of TGF-(3 signaling. Our results establish the metabolic basis of EndMT persistence and unveil novel targets, such as ACSS2, for the potential treatment of chronic vascular diseases.
Cell Biology Endocrinology & Metabolism Life Sciences & Biomedicine Science & Technology

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