Clinical Report: Lactylation in Atherosclerosis Development and Treatment
Overview
This review highlights the role of lactylation, a post-translational modification, in the development of atherosclerosis (AS) through its regulation of key pathological processes.
Background
Atherosclerosis is a significant contributor to cardiovascular morbidity and mortality, necessitating a deeper understanding of its underlying mechanisms. Lactylation, involving the addition of lactate-derived lactyl groups to proteins, has emerged as a crucial factor in the pathophysiology of AS.
Data Highlights
No numerical data or trial results were provided in the source material.
Key Findings
Lactylation is a post-translational modification that affects protein function and stability.
It plays a role in vascular inflammation, endothelial-to-mesenchymal transition, and angiogenesis in AS.
Histone acetyltransferase p300 and CREB-binding protein (CBP) are identified as lactyltransferases.
Delactylases, including class I histone deacetylases, may regulate lactylation by removing lactyl groups.
Clinical Implications
Clinicians should consider the role of lactylation in the pathogenesis of atherosclerosis when evaluating patients.
Conclusion
Lactylation represents a significant epigenetic and metabolic factor in atherosclerosis.
