Fig. 3

Schematic diagram of the role of lactate in heart failure, myocardial infarction, atrial fibrillation and atherosclerosis. In heart failure, the increase in lactate levels in myocardial cells can improve myocardial metabolism through the pyruvate-lactate axis, thereby improving myocardial hypertrophy. In addition, recent studies have found that α-MHC-K1897la lactylation can improve sarcomeric structure and function, thereby alleviating the development of heart failure. Furthermore, lactate can regulate the production of inflammatory cytokines by myocardial fibroblasts, reducing the production of Fas, Fraktalkine, or IL-12p40 and stimulating IL-13 and SDF1a to improve heart failure. It is unclear whether lactylation in myocardial fibroblasts involve in heart failure. In myocardial infarction, the early increase in the level of H3K18la in monocytes can promote the expression of repair genes (Lrg1, Vegf-α, and IL-10), thereby improving myocardial infarction. In addition, in the later stage, the increase in snail1 lactylation in vascular endothelial cells can promote the expression of tfg genes, thereby promoting the occurrence of EndMT and exacerbating the occurrence of myocardial infarction. In atrial fibrillation, high level of lactate can stimulate myocardia cells to produce ROS and cause myocardia cells apoptosis. It is unclear whether lactylation in myocardial fibroblasts involve in atrial fibrillation. In atherosclerosis, lactate can promote the proliferation and migration of smooth muscle cells and phenotypic transformation, thus promoting the occurrence of atherosclerosis. The increased level of Mecp2-k271la in vascular endothelial cells can inhibit the expression of the Ereg gene and the production of inflammatory mediators (IL-6, IL-1β, and VCAM-1), thereby inhibiting the occurrence of atherosclerosis. At present, it is not clear whether lactate can affect the occurrence of atherosclerosis by affecting histone or nonhistone lactylation or by other unknown mechanisms in macrophages. Abbreviations: EndMT: endothelial-to-mesenchymal transition