Related Experiment Video
Updated: May 4, 2026

Methyl-binding DNA capture Sequencing for Patient Tissues
Published on: October 31, 2016
A comprehensive review of m6 A methylation in coronary heart disease
Mei-Ning Diao1,2, Yi-Jv Lv1,2, Hui Xin1
1Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, 266000, Shandong, P. R. China.
Insights
m6A methylation, an RNA modification, plays a key role in coronary heart disease (CHD) development. Targeting m6A regulators offers a promising avenue for early CHD detection and novel therapeutic strategies.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Epigenetics
Background:
- Coronary heart disease (CHD) poses a significant global health burden, primarily driven by coronary atherosclerosis (AS).
- AS involves chronic inflammation and cellular changes within coronary vessels.
- RNA modifications, like m6A methylation, are emerging as critical factors in disease pathogenesis.
Purpose of the Study:
- To investigate the role of m6A methylation in the development and progression of coronary heart disease (CHD).
- To explore the potential of m6A regulators as diagnostic markers and therapeutic targets for CHD.
Main Methods:
- Review of current research on m6A methylation and its regulators in the context of atherosclerosis and CHD.
- Analysis of how m6A modification influences key pathological processes in CHD, including inflammation, cell death, and fibrosis.
Main Results:
- m6A methylation regulators are implicated in the pathogenesis of AS, influencing inflammatory responses and cellular proliferation.
- Dysregulation of m6A pathways contributes to myocardial ischemia and infarction.
- m6A profiling shows potential for early CHD diagnosis.
Conclusions:
- m6A methylation is a crucial player in the intricate processes underlying CHD.
- m6A regulators represent promising targets for developing novel diagnostic tools and therapeutic interventions for CHD.
Abstract:
The morbidity and mortality rates of coronary heart disease (CHD) are high worldwide. The primary pathological changes in CHD involve stenosis and ischemia caused by coronary atherosclerosis (AS). Extensive research on the pathogenesis of AS has revealed chronic immunoinflammatory processes and cell proliferation in all layers of coronary vessels, including endothelial cells (ECs), vascular smooth muscle cells, and macrophages. m6 A methylation is a common posttranscriptional modification of RNA that is coordinated by a variety of regulators (writers, readers, erasers) to maintain the functional stability of modified mRNAs and ncRNAs. In recent years, there has been increasing focus on the involvement of m6 A methylation in the incidence and progression of CHD, which starts with atherosclerotic plaque formation, leads to myocardial ischemia, and ultimately results in the occurrence of myocardial infarction (MI). m6 A regulators modulate relevant signaling pathways to participate in the inflammatory response, programmed death of cardiomyocytes, and fibrosis. Therefore, diagnostic models based on m6 A profiling are helpful for the early detection of CHD, and m6 A methylation shows promise as a sensitive target for new drugs to treat CHD in the future.
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