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<p>Ischemic heart disease (IHD), especially acute myocardial infarction (AMI), has a high mortality rate and poses a great threat to human health. When myocardial infarction occurs, the structure and function of the myocardium are significantly damaged, and its metabolisms switch from oxidative phosphorylation to glycolysis, producing lactate. Lactylation, as a newly discovered post-translational modification (PMT) in recent years, is involved in the regulation of gene expression, and cell proliferation. Emerging studies have revealed that lactate and lactylation modifications participate in inflammation and cardiac repair, and play an important role in cardiovascular diseases, such as myocardial infarction, myocardial fibrosis, and heart failure. Therefore, in this review, we discuss how glucose metabolism, glycolytic end-product lactate, and lactylation potentially interact with pathological processes, including inflammation, cardiac fibrosis, and heart failure. And targeting glycolysis and lactylation modification could provide a promising future for cardiovascular diseases.</p> Graphical Abstract <p>Cardiovascular diseases significantly alter cardiac structure and metabolism.&#xa0;Lactic acid, the byproduct of glycolysis, and its associated lactylation modification act&#xa0;as modulators that influence outcomes and prognosis of diseases. In this review, we&#xa0;discussed how glucose metabolism, lactate, and lactylation are involved in the&#xa0;pathophysiological processes of myocardial infarction. When myocardial infarction&#xa0;occurs, the structure and function of the myocardium are significantly damaged, and&#xa0;its metabolisms switch from oxidative phosphorylation to glycolysis, producing&#xa0;lactate. And newly discovered post-translational modification lactylation, which uses&#xa0;lactate as substrates, is involved in the regulation of gene expression, and cell&#xa0;proliferation. And we summarize and conclude that lactate and lactylation&#xa0;post-myocardial infarction can participate in inflammation, fibrosis, and&#xa0;heart failure. Meanwhile, we provide a promising targeted therapy for ischemic heart&#xa0;disease through metabolic regulation and epigenetic modification.</p>

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Targeting Lactic Acid Modification in Ischemic Heart Diseases: Novel Therapeutics and Mechanism

  • 期刊论文

  • 发表日期：

    2025年2月7日

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  • Tangjiang Wan,
  • Yucheng Liang,
  • Tianwen Wei,
  • Zijie Chen,
  • Yafei Li

摘要

Ischemic heart disease (IHD), especially acute myocardial infarction (AMI), has a high mortality rate and poses a great threat to human health. When myocardial infarction occurs, the structure and function of the myocardium are significantly damaged, and its metabolisms switch from oxidative phosphorylation to glycolysis, producing lactate. Lactylation, as a newly discovered post-translational modification (PMT) in recent years, is involved in the regulation of gene expression, and cell proliferation. Emerging studies have revealed that lactate and lactylation modifications participate in inflammation and cardiac repair, and play an important role in cardiovascular diseases, such as myocardial infarction, myocardial fibrosis, and heart failure. Therefore, in this review, we discuss how glucose metabolism, glycolytic end-product lactate, and lactylation potentially interact with pathological processes, including inflammation, cardiac fibrosis, and heart failure. And targeting glycolysis and lactylation modification could provide a promising future for cardiovascular diseases.

Graphical Abstract

Cardiovascular diseases significantly alter cardiac structure and metabolism. Lactic acid, the byproduct of glycolysis, and its associated lactylation modification act as modulators that influence outcomes and prognosis of diseases. In this review, we discussed how glucose metabolism, lactate, and lactylation are involved in the pathophysiological processes of myocardial infarction. When myocardial infarction occurs, the structure and function of the myocardium are significantly damaged, and its metabolisms switch from oxidative phosphorylation to glycolysis, producing lactate. And newly discovered post-translational modification lactylation, which uses lactate as substrates, is involved in the regulation of gene expression, and cell proliferation. And we summarize and conclude that lactate and lactylation post-myocardial infarction can participate in inflammation, fibrosis, and heart failure. Meanwhile, we provide a promising targeted therapy for ischemic heart disease through metabolic regulation and epigenetic modification.