Key result
Lactate and lactylation influence ischemic cardiomyopathy pathophysiology via epigenetic changes, offering potential therapeutic targets.
Why the study?
The role of lactylation, an emerging epigenetic modification, and lactate accumulation in the pathophysiology, gene expression, and cellular signaling of ICM remained to be comprehensively analyzed.
This review highlights the emerging role of lactylation as an epigenetic modification in ischemic cardiomyopathy, offering potential new targets for future research.
Hypothesis-generating for lactylation-targeted therapies in ischemic cardiomyopathy; prospective validation required before clinical adoption.
Ischemic cardiomyopathy (ICM) is a significant global public health issue, with its pathophysiology encompassing atherosclerotic plaque formation, thrombosis, hypoperfusion, ischemic cell death, and left ventricular remodeling. Lactate is not only regarded as an energy metabolite but also acts as a signaling molecule that influences various physiological processes, regulating metabolism and muscle contraction. Lactylation, an emerging epigenetic modification, affects protein functionality and gene expression through the P300 enzyme. In ICM, lactate accumulation leads to pH imbalance and myocardial cell dysfunction, impacting cellular signaling. This paper will analyze the role of lactylation in ICM, focusing on coronary artery disease (ASCVD) and myocardial infarction (MI). It will also explore the differential expression and immunological characteristics of lactylation-related genes in normal and ICM tissues, providing potential targets for future research.
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Zhang et al. (2025) conducted a review in Ischemic cardiomyopathy. Lactate and lactylation vs. Normal tissues was evaluated on Differential expression and immunological characteristics of lactylation-related genes. Lactate and lactylation influence ischemic cardiomyopathy pathophysiology through epigenetic modifications and gene expression, offering potential therapeutic targets.
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