ArticleCells2022
Exploration of N6-Methyladenosine Profiles of mRNAs and the Function of METTL3 in Atherosclerosis.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- The Complex Role of Methylation in Regulating Vascular Smooth Muscle Cell Phenotypic States in Vascular Remodeling and Atherosclerosis.Biomolecules · 2026Review
- The Critical Roles of Methyltransferase-Like 3 in Atherosclerosis and Arterial Infarction: Breakthroughs in Mechanism Understanding.Journal of cellular and molecular medicine · 2025Review
- Emerging mechanisms and implications of m6A in CVDs: potential applications of natural products.Frontiers in cardiovascular medicine · 2025Review
- Insights into RNA N6-methyladenosine and programmed cell death in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Transcriptome-wide NBMC genomics · 2023Article
- mActa biochimica et biophysica Sinica · 2023Review
- METTL3: a Potential New Target in the Treatment Strategy of Atherosclerosis?Cardiovascular drugs and therapy · 2023Article
- The cellular uncertainty in thoracic aortic dissections: the roles of METTL3 and NOTCH1 on m6A in human aortic smooth muscle cells.Annals of translational medicine · 2023Article
- The Epigenetic Regulation of RNA N6-Methyladenosine Methylation in Glycolipid Metabolism.Biomolecules · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesN6-methylladenosine (m6A) modification has not been fully studied in atherosclerosis. The objectives of this study were to investigate differentially expressed m6A methylated peaks and mRNAs, along with the regulatory role of methyltransferase 3 (METTL3) in pathological processes of atherosclerosis.
methodsThe pathological models of human coronary artery smooth muscle cells (HCASMCs) were induced in vitro. The differentially expressed mRNAs and m6A peaks were identified by RNA-Seq and meRIP-Seq. The potential mechanisms were analyzed via bioinformatic assays. Methylases expression was tested by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) in HCASMCs, and by immunohistochemical assays in 40 human coronary arteries. The knockdown of METTL3 expression in cells was performed by siRNA transfection, and cell proliferation and migration were detected after transfection.
resultsWe identified 5121 m6A peaks and 883 mRNAs that were expressed differentially in the pathological processes of HCASMCs. Bioinformatic analyses showed that the different m6A peaks were associated with cell growth and cell adhesion, and the 883 genes showed that the extracellular matrix and PI3K/AKT pathway regulate the processes of HCASMCs. Additionally, 10 hub genes and 351 mRNAs with differential methylation and expression levels were found. METTL3 was upregulated in the arteries with atherosclerotic lesions and in the proliferation and migration model of HCASMCs, and pathological processes of HCASMCs could be inhibited by the knockdown of METTL3. The mechanisms behind regulation of migration and proliferation reduced by siMETTL3 are concerned with protein synthesis and energy metabolism.
conclusionsThese results revealed a new m6A epigenetic method to regulate the progress of atherosclerosis, which suggest approaches for potential therapeutic interventions that target METTL3 for the prevention and treatment of coronary artery diseases.
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