The glucose-to-acetate metabolic flux that drives endothelial-to-mesenchymal transition via TGF-β signaling.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 37437542.
- Also identified by DOI 10.1016/j.cmet.2023.06.006.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
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.
Medical subject headings
- Acetates
- Atherosclerosis
- Glucose
- Transforming Growth Factor beta