ArticleCardiovascular drugs and therapy2023
Silencing METTL3 Stabilizes Atherosclerotic Plaques by Regulating the Phenotypic Transformation of Vascular Smooth Muscle Cells via the miR-375-3p/PDK1 Axis.
Article in Cardiovascular drugs and therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Vascular smooth muscle cell FTO deletion aggravates atherosclerotic plaque instability by promoting VSMC migration through the NScience China. Life sciences · 2026Article
- mBiomolecules · 2026Review
- METTL14 inhibits atherogenesis by epigenetically activating PPAR-α/γ transcription and fatty acid oxidation in VSMCs.Cardiovascular research · 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
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- MiR-375 Targeting PDK1 Regulates the Wnt/β-Catenin Pathway in Lower Extremity Arteriosclerosis Obliterans.Vascular health and risk management · 2026Article
- PARP1 contributes to intimal hyperplasia by regulating METTL3-mediated m6A methylation of TRAIL.Cell biology and toxicology · 2025Article
- The Critical Roles of Methyltransferase-Like 3 in Atherosclerosis and Arterial Infarction: Breakthroughs in Mechanism Understanding.Journal of cellular and molecular medicine · 2025Review
- Phenotypic switching of vascular smooth muscle cells: a central mechanism in vein graft intimal hyperplasia.Frontiers in cardiovascular medicine · 2025Review
- Deciphering single-cell landscape unravels cell-type-specific functional roles of RNA mTheranostics · 2025Article
- Recent Advances in the Mutual Regulation of m6A Modification and Non-Coding RNAs in Atherosclerosis.International journal of general medicine · 2025Review
- NAging and disease · 2024Review
- Oral Nanoformulations in Cardiovascular Medicine: Advances in Atherosclerosis Treatment.Pharmaceuticals (Basel, Switzerland) · 2024Review
- N6-methyladenosine-driven miR-143/145-KLF4 circuit orchestrates the phenotypic switch of pulmonary artery smooth muscle cells.Cellular and molecular life sciences : CMLS · 2024Article
- RNA modifications in cellular metabolism: implications for metabolism-targeted therapy and immunotherapy.Signal transduction and targeted therapy · 2024Review
- N6-Methyladenosine in Cell-Fate Determination of BMSCs: From Mechanism to Applications.Research (Washington, D.C.) · 2024Article
- PCSK9i promoting the transformation of AS plaques into a stable plaque by targeting the miR-186-5p/Wipf2 and miR-375-3p/Pdk1/Yap1 in ApoE-/- mice.Frontiers in medicine · 2024Article
- Colchicine Blocks Abdominal Aortic Aneurysm Development by Maintaining Vascular Smooth Muscle Cell Homeostasis.International journal of biological sciences · 2024Article
- Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications.Frontiers in cardiovascular medicine · 2024Review
- mActa biochimica et biophysica Sinica · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAtherosclerosis (AS) is a primary cause of cardiovascular diseases. This study investigated the mechanism of methyltransferase-like 3 (METTL3) in AS plaques via modulating the phenotypic transformation of vascular smooth muscle cells (VSMCs).
methodsAS mouse models and MOVAS cell models were established through high-fat diet and the treatment of ox-LDL, respectively. METTL3 expression in AS models was detected via RT-qPCR and Western blot. The AS plaques, lipid deposition, and collagen fibers were examined via histological staining. The levels of Ly-6c, α-SMA, and OPN were examined via Western blot. The blood lipid indexes in mouse aortic tissues were determined using kits. The proliferation and migration of MOVAS cells were detected via CCK-8 and Transwell assays. The m
resultsMETTL3 was highly expressed in AS. Silencing METTL3 alleviated AS progression and stabilized AS plaques in mice, and limited the phenotypic transformation of VSMCs induced by ox-LDL. Silencing METTL3 inhibited m
conclusionMETTL3-mediated m
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.