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Updated: May 29, 2025

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Targeting Lactic Acid Modification in Ischemic Heart Diseases: Novel Therapeutics and Mechanism
Tangjiang Wan1, Yucheng Liang1, Tianwen Wei2
1Department of Cardiology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, 215000, Jiangsu Province, China.
Insights
Acute myocardial infarction (AMI) damages heart function, shifting metabolism to produce lactate. Lactylation, a new modification, plays a role in inflammation and repair, offering potential therapeutic targets for heart disease.
Area of Science:
- Biochemistry
- Cardiology
- Molecular Biology
Background:
- Ischemic heart disease (IHD), particularly acute myocardial infarction (AMI), presents a significant global health challenge with high mortality rates.
- Myocardial infarction leads to substantial damage to heart structure and function, altering cellular metabolism from oxidative phosphorylation to glycolysis, resulting in lactate production.
Purpose of the Study:
- To explore the intricate relationship between glucose metabolism, lactate, and lactylation in the context of cardiovascular diseases.
- To elucidate the roles of lactate and lactylation in pathological processes such as inflammation, cardiac fibrosis, and heart failure following myocardial infarction.
Main Methods:
- This review synthesizes current research on glucose metabolism shifts in myocardial infarction.
- It examines the emerging role of lactylation as a post-translational modification.
- The review analyzes studies investigating the involvement of lactate and lactylation in cardiovascular disease pathogenesis.
Main Results:
- Lactate, a byproduct of altered glucose metabolism during myocardial infarction, and lactylation modifications are increasingly recognized for their involvement in inflammation and cardiac repair.
- Emerging evidence highlights their significant roles in cardiovascular conditions including myocardial infarction, fibrosis, and heart failure.
Conclusions:
- Targeting glycolysis and lactylation modifications presents a promising therapeutic avenue for managing cardiovascular diseases.
- Understanding these metabolic and post-translational modifications is crucial for developing novel treatment strategies for heart conditions.
Abstract:
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.
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