Glycolysis is an important way for various cells such as vascular wall endothelial cells, smooth muscle cells, macrophages, and other cells to obtain energy. In pathological conditions, it can participate in the process of AS by regulating lipid deposition, calcification, angiogenesis in plaques, etc., together with its metabolite lactic acid. Recent studies have shown that lactate-related lactylation modifications are ubiquitous in the human proteome and are involved in the regulation of various inflammatory diseases. Combined with the distribution and metabolic characteristics of cells in the plaque in the process of AS, glycolysis-lactate-lactylation modification may be a new entry point for targeted intervention in atherosclerosis in the future. Therefore, this article intends to elaborate on the role and mechanism of glycolysis-lactate-lactylation modification in AS, as well as the opportunities and challenges in targeted therapy, hoping to bring some help to relevant scholars in this field. In atherosclerosis, glycolysis, lactate, and lactylation modification as a metabolic sequence affect the functions of macrophages, smooth muscle cells, endothelial cells, lymphocytes, and other cells and interfere with processes such as vascular calcification and intraplaque neovascularization to influence the progression of atherosclerosis.
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