Lactylation: a metabolic–epigenetic driver in atherosclerosis pathogenesis and therapeutic targeting

Category	Detail
Condition	Atherosclerosis
Key Mechanisms	Lactylation regulates inflammation, epithelial–mesenchymal transition, angiogenesis, vascular smooth muscle cell senescence, and metabolic dysregulation.
Target Population	Individuals at risk for cardiovascular diseases, including those with hypercholesterolemia, hypertension, diabetes, and obesity.
Care Setting	Clinical research and cardiovascular disease management.

Lactylation is a post-translational modification that affects protein function and stability.
It plays a crucial role in the initiation and progression of atherosclerosis.
Key pathological processes influenced by lactylation include vascular inflammation and metabolic dysregulation.
Lactyltransferases and delactylases are critical in regulating lactylation levels.
Understanding lactylation may lead to novel therapeutic strategies for atherosclerosis.

Identify risk factors for atherosclerosis, including hypercholesterolemia and hypertension.

Target lactylation pathways as potential therapeutic interventions in atherosclerosis.

Monitor inflammatory markers and metabolic profiles in patients with atherosclerosis.

Chronic exposure to risk factors can exacerbate vascular inflammation and accelerate atherosclerosis progression.

Patients with atherosclerosis and related cardiovascular conditions.

Lactylation-targeted interventions may slow disease progression and reduce cardiovascular events.

Incorporate assessment of lactylation in the evaluation of atherosclerosis.
Consider metabolic and inflammatory profiles in the management of cardiovascular diseases.

Clinical Scorecard: Lactylation: An Epigenetic and Metabolic Factor in the Development and Treatment of Atherosclerosis