The glucose-to-acetate metabolic flux that drives endothelial-to-mesenchymal transition via TGF-β signaling

Cristina Arce Recatalá; Massimo M Santoro

doi:10.1016/j.cmet.2023.06.006

The glucose-to-acetate metabolic flux that drives endothelial-to-mesenchymal transition via TGF-β signaling

Cell Metab. 2023 Jul 11;35(7):1093-1095. doi: 10.1016/j.cmet.2023.06.006.

Authors

Cristina Arce Recatalá¹, Massimo M Santoro²

Affiliations

¹ Laboratory of Angiogenesis and Cancer Metabolism, Department of Biology, University of Padua, Padua, Italy, 35131.
² Laboratory of Angiogenesis and Cancer Metabolism, Department of Biology, University of Padua, Padua, Italy, 35131. Electronic address: massimo.santoro@unipd.it.

PMID: 37437542
DOI: 10.1016/j.cmet.2023.06.006

Abstract

The metabolic mechanisms supporting the process of endothelial-to-mesenchymal transition (EndMT) remain largely unknown. Here, Zhu et al. describe a novel role for acetate and ACC2 in regulating EndMT and atherosclerosis via modulation of the TGF-β signaling. This study sheds light on the role of glucose-derived metabolites that drive endothelial pathophysiology.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Acetates* / metabolism
Atherosclerosis*
Glucose*
Humans
Transforming Growth Factor beta* / metabolism

Substances

Acetates
Glucose
Transforming Growth Factor beta