Abstract
The metabolic mechanisms supporting the process of endothelial-to-mesenchymal transition (EndMT) remain largely unknown. Here, Zhu etal. 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.
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