Modulating specific components of the lactylation pathway may offer therapeutic opportunities to influence cardiac repair outcomes following myocardial injury.
This review highlights the emerging role of lactylation, a lactate-driven post-translational modification, in regulating cellular processes during cardiac repair following myocardial injury.
Lactylation is a lactate-driven post-translational modification that directly modifies lysine residues on both histone and non-histone proteins, thereby linking energy metabolism to epigenetic regulation. Its levels are dynamically orchestrated by intracellular lactate availability, as well as by specific lactyltransferases and delactylases, including p300, histone deacetylases (HDACs), and sirtuin family members. The functional significance of lactylation is increasingly recognized in cardiovascular disease, particularly in the context of cardiac repair. Lactylation has been implicated in multiple facets of cardiac repair, including macrophage polarization, endothelial-to-mesenchymal transition, fibroblast activation, and cardiomyocyte survival. Dysregulation of lactylation across various cardiac cell types following myocardial injury suggests that modulating specific components of this modification pathway may offer therapeutic opportunities to influence repair outcomes. This review synthesizes current knowledge on the cell-specific functions of lactylation in cardiac repair and its regulatory networks, with the goal of identifying potential diagnostic markers and therapeutic targets.
Guo et al. (Fri,) conducted a review in Cardiovascular disease. Lactylation modulation was evaluated. Modulating specific components of the lactylation pathway may offer therapeutic opportunities to influence cardiac repair outcomes following myocardial injury.