Objective:

To summarize the molecular mechanisms through which lactylation contributes to the initiation and progression of atherosclerosis (AS).

Approach:

• Lactylation Mechanism Overview: Lactylation involves the addition of lactate-derived lactyl groups to lysine residues on proteins, affecting their function and stability.
• Role in Atherosclerosis: The review discusses lactylation's involvement in key pathological processes of AS, including inflammation, endothelial–mesenchymal transition, angiogenesis, and vascular smooth muscle cell senescence.

Key Findings:

• Lactylation regulates several pathological processes associated with atherosclerosis.
• Lactate is converted into lactyl-CoA, which is transferred to proteins by lactyltransferases.
• Histone acetyltransferase p300 may act as a lactyltransferase, influencing histone lactylation.
• Delactylases, such as certain histone deacetylases, may remove lactyl groups, regulating lactylation.

Interpretation:

Lactylation plays a significant role in the pathophysiology of atherosclerosis, linking metabolic dysregulation and epigenetic changes.

Limitations:

• The review lacks a systematic discussion of lactylation's specific roles in atherosclerosis compared to other modifications.
• Further research is needed to fully elucidate the context-dependent effects of lactylation.

Conclusion:

Understanding lactylation's role in atherosclerosis may lead to novel therapeutic strategies targeting this modification.