Why the study?
High lactate levels are linked to prognosis and mortality after myocardial infarction, and endothelial-to-mesenchymal transition contributes to cardiac fibrosis, but the mechanistic role of lactate remained unknown.
Does lactate promote endothelial-to-mesenchymal transition and cardiac fibrosis following myocardial infarction?
Population
Endothelial cells and post-myocardial infarction models
Comparison
Lactate treatment, Snail1 inhibition, CHC, or MCT1 silencing vs controls
Design
Preclinical mechanistic study
Authors
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Lactate may drive post-MI fibrosis via EndoMT in animal models; leaves open whether MCT or lactylation inhibition improves human outcomes.
Does lactate promote endothelial-to-mesenchymal transition and cardiac fibrosis following myocardial infarction?
Lactate acts as a signaling molecule that exacerbates post-MI cardiac fibrosis and dysfunction by promoting endothelial-to-mesenchymal transition via Snail1 lactylation.
Fan et al. (2023) studied this question.
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