Epigenetics Unlocks New Clues in the Fight Against Atherosclerosis

Atherosclerosis remains the leading cause of cardiovascular disease worldwide. New research highlights the critical role of epigenetic mechanisms in its development and progression. Epigenetic changes deeply affect the behaviour of cells within arterial walls. In vascular endothelial cells, these modifications alter barrier function, inflammation, and responses to blood flow stress, which are key in early plaque formation. Vascular smooth muscle cells also undergo epigenetic reprogramming, allowing them to switch phenotypes and reshape the extracellular matrix.

Immune cells in atherosclerotic plaques experience significant epigenetic modulation. This influences their activation and inflammatory responses, shaping disease progression. Histone modifications further control gene accessibility within these plaques, adding another layer of regulation.

Non-coding RNAs, such as lncRNAs and miRNAs, contribute to this complexity. They interact with other epigenetic marks, including DNA methylation, which governs cell proliferation and inflammation. Multi-omics techniques now allow scientists to untangle these cell-specific contributions in greater detail.

Preclinical trials have begun testing drugs that target epigenetic pathways. Early results suggest these compounds may reduce plaque buildup and vascular inflammation. Epigenetic processes are now recognised as central to atherosclerosis. They influence every stage, from initial vascular changes to immune cell behaviour in established plaques. Targeting these mechanisms could lead to new therapies for reducing the global burden of cardiovascular disease.