Epigenetic‑ncRNA crosstalk in atherosclerosis: Mechanisms, disease progression and therapeutic potential (Review).

Abstract

Atherosclerosis is a chronic and progressive vascular disease involving the gradual accumulation of lipids, cholesterol, cellular debris, and fibrous elements within the arterial wall. This process leads to the thickening and hardening of arteries, resulting in restricted blood flow and reduced oxygen delivery to tissues. Over time, these pathological changes significantly elevate the risk of life‑threatening cardiovascular events, including myocardial infarction and ischemic stroke. Recent studies emphasize the significant role of epigenetic modifications and non‑coding RNAs (ncRNAs) in regulating the progression of atherosclerosis. Histone modifications, DNA methylation, and ncRNAs interact to modulate gene expression, influencing endothelial dysfunction, lipid metabolism, and inflammatory processes. Epigenetic regulators, such as DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), control key vascular genes, while ncRNAs like microRNAs (miRNAs), long non‑coding RNAs (LncRNAs), and circular RNAs (circRNAs) contribute to the modulation of cholesterol efflux and foam cell formation. Understanding the complex interplay between these molecular pathways offers new therapeutic insights for managing atherosclerosis and its complications. The reversible nature of epigenetic changes, alongside ncRNA‑based therapies, holds promising potential for future clinical applications, though challenges such as delivery mechanisms and specificity remain.