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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis [1]

ABSTRACT: Acetate controls endothelial-to-mesenchymal transition during atherosclerosis [1]

PROVIDER: PRJNA933103 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23379674_1.fastq.gz	Fastqsanger.gz
	SRR23379674_2.fastq.gz	Fastqsanger.gz
	SRR23379675_1.fastq.gz	Fastqsanger.gz
	SRR23379675_2.fastq.gz	Fastqsanger.gz
	SRR23379676_1.fastq.gz	Fastqsanger.gz

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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis

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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis [2]

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Acetate controls endothelial-to-mesenchymal transition during atherosclerosis

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Acetate controls endothelial-to-mesenchymal transition.

Project description:Endothelial-to-mesenchymal transition (EndMT), a process initiated by activation of endothelial TGF-β signaling, underlies numerous chronic vascular diseases and fibrotic states. Once induced, EndMT leads to a further increase in TGF-β 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-β-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-β-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-β receptor ALK5 and SMADs 2 and 4 leading to activation and long-term stabilization of TGF-β 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.

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BW25113 glucose to acetate transition

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