Key result
The mutual regulation between m6A modifications and non-coding RNAs plays a pivotal role in the pathogenesis of atherosclerosis by modulating lipid metabolism, inflammation, and endothelial function.
Why the study?
Understanding the mutual regulation between m6A modifications and non-coding RNAs is of great significance to identify novel therapeutic targets for atherosclerosis.
Understanding the mutual regulation between m6A modifications and non-coding RNAs provides insights into the epigenetic mechanisms of atherosclerosis and may identify novel therapeutic targets.
Should not yet influence cardiovascular risk assessment or treatment; leaves open a novel epigenetic pathway for future atherosclerosis.
Atherosclerosis, a progressive inflammatory disease of the arteries, remains a leading cause of cardiovascular morbidity and mortality worldwide. Recent years have witnessed the pivotal role of N6-methyladenosine (m6A) RNA methylation in regulating various biological processes, including those implicated in atherosclerosis. Current evidence suggested that m6A regulators (writers, erasers, and readers) participated in the modification of multiple non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), thereby affecting their metabolism and functions. Meanwhile, ncRNAs have also emerged as key modulator of m6A regulators expression in turn. Therefore, understanding the mutual regulation between m6A modifications and ncRNAs is of great significance to identify novel therapeutic targets for atherosclerosis and has great clinical application prospects. This review aims to summarize the recent advances in the reciprocal regulation and provide insights into the interaction between m6A modification and ncRNAs in the context of atherosclerosis.
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Wang et al. (2025) conducted a review in Atherosclerosis. m6A modification and non-coding RNAs was evaluated. The mutual regulation between m6A modifications and non-coding RNAs plays a pivotal role in the pathogenesis of atherosclerosis by modulating lipid metabolism, inflammation, and endothelial function.
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