Epigenetic Alterations Induced by Air Pollution: A Key Driver in Atherosclerosis Development

Air pollution, a global health concern, is linked to atherosclerosis through epigenetic modifications such as DNA methylation, histone modifications, and non-coding RNA regulation. Long-term exposure to air pollution such as particulate matter 2.5 (PM 2.5), polycyclic aromatic hydrocarbons (PAHs), and heavy metals can induce alterations in DNA methylation patterns, especially in genes regulating inflammation and cholesterol metabolism, contributing to atherosclerosis development. DNA methylation plays a fundamental role in regulating gene expression by silencing or activating genes involved in endothelial dysfunction, inflammation, and lipid metabolism, all of which contribute to atherosclerosis progression. Moreover, it explores the influence of air pollution on histone modifications, emphasizing their role in pathways critical to atherosclerotic progression. Histone modifications, such as acetylation and methylation, alter chromatin structure and gene accessibility, impacting key signaling pathways related to vascular inflammation and plaque formation. It explores the interconnection between air pollution and non-coding RNA (ncRNA) modifications, shedding light on the significance of miRNAs and lncRNAs as potential biomarkers indicative of cardiovascular susceptibility triggered by exposure to particulate matter (PM). Non-coding RNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), modulate post-transcriptional gene regulation, influencing inflammatory responses, oxidative stress, and endothelial function in atherosclerosis. Understanding these epigenetic changes is vital for developing strategies to mitigate air pollution's impact on cardiovascular health.