ArticleCardiovascular research2025
Methyltransferase-like 3-catalysed N6-methyladenosine methylation facilitates the contribution of vascular smooth muscle cells to atherosclerosis.
Article in Cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Article
- Vascular smooth muscle cell FTO deletion aggravates atherosclerotic plaque instability by promoting VSMC migration through the NScience China. Life sciences · 2026Article
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- METTL3/YTHDC1 axis-mediated mMolecular medicine (Cambridge, Mass.) · 2026Article
- N6-methyladenosine (m6A) post-transcriptional modification regulation of mRNA, an overlooked therapeutic opportunity to leverage mRNA processing in vascular smooth muscle cells.Vascular pharmacology · 2026Review
- Mitochondrial homeostasis: the central hub governing the progression of atherosclerosis.Precision clinical medicine · 2026Review
- ZIKV NS3 disrupts Nrf2-mediated antioxidant defense and drives vascular smooth muscle cell damage and vascular dysfunction.Zoological research · 2026Article
- RNA methylation in cardiovascular remodeling: Molecular mechanisms, biomarkers, and therapeutic strategies.Molecular biology reports · 2026Review
- Transcriptome-Wide Analysis of N6-Methyladenosine Modification in the Liver of Geese at Different Growth Stages.Animals : an open access journal from MDPI · 2026Article
- A Comprehensive Review of Epigenetic Regulation of Vascular Smooth Muscle Cells During Development and Disease.Biomolecules · 2026Review
- MFrontiers in genetics · 2026Review
- Sesamin attenuates atherosclerosis by alleviating vascular endothelial ferroptosis-related injuryFrontiers in cell and developmental biology · 2026Article
- Macrophage-derived semaphorin 7A drives atherosclerosis via the integrin β1/JNK/MSR1 axis.Frontiers of medicine · 2025Article
- Macrophage-like smooth muscle cells in atherosclerosis.Molecular biology reports · 2025Review
- Novel role of vascular smooth muscle cell-expressed METTL3 in atherosclerosis.Cardiovascular research · 2025Article
- Research progress on the application of nanoparticles delivery in the treatment of atherosclerosis: implications for therapeutic interventions.Frontiers in cell and developmental biology · 2025Review
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14 authors.
Funding
Abstract
aimsVascular smooth muscle cells (VSMCs) are involved in the aetiology of atherosclerosis, but whether methyltransferase-like 3 (METTL3)-catalysed N6-methyladenosine (m6A) modulates the contribution of VSMCs to atherosclerosis remains elusive. METHODS AND
resultsWe generated tamoxifen-inducible VSMC-specific METTL3 knockout mice with VSMC lineage tracing and found that VSMC-specific METTL3 deficiency substantially attenuated atherosclerosis and reduced the proportion of VSMCs in plaques, due to the inhibition of VSMC atheroprone phenotype as characterized by macrophage-like and inflammatory features as well as high migratory and proliferative capacity. m6A-methylated RNA immunoprecipitation sequencing (MeRIP-Seq) combined with polysome profiling analysis mechanistically displayed METTL3-catalysed m6A methylation of myocardin-related transcription factor A (MRTFA) mRNA and further enhanced YTH N6-methyladenosine RNA-binding protein F3 (YTHDF3)-dependent MRTFA mRNA translation. Conversely, adenovirus or adeno-associated virus-mediated VSMC-specific MRTFA overexpression abolished METTL3 deficiency-mediated alleviation of VSMC atheroprone phenotypic switching and atherosclerotic progression both in vitro and in vivo.
conclusionMETTL3 facilitated the contribution of VSMCs to atherosclerosis through the m6A-YTHDF3-dependent MRTFA mRNA translation enhancement.
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