Review highlights lactate and lactylation influence immune functions in atherosclerosis, suggesting therapeutic targets.
Atherosclerosis is a leading cause of cardiovascular diseases, causing significant morbidity and mortality. This review article examines the role of lactate and lactylation in atherosclerosis, a chronic inflammatory disease closely linked to lipid metabolism and immune system activation. Lactate, a metabolic byproduct and signaling molecule, has emerged as a key regulator of immune cell functions and epigenetic modifications. The article explores the mechanisms through which lactate and lactylation influence macrophage polarization, T‑cell differentiation and B‑cell metabolism, highlighting their complex dual roles in the progression of atherosclerosis. By modulating metabolic reprogramming, functional polarization and epigenetic regulation, lactate and lactylation significantly impact plaque formation and stability. These findings provide a foundation for developing novel therapeutic strategies targeting lactate metabolism and lactylation pathways.
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Xiong et al. (2025) studied this question.
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