ArticleCellular & molecular biology letters2022
METTL3 mediates Ang-II-induced cardiac hypertrophy through accelerating pri-miR-221/222 maturation in an m6A-dependent manner.
Article in Cellular & molecular biology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 87 citations in OpenAlex.
- N6-methyladenosine modification of NEU1 mediated by METTL3 exacerbates angiotensin II-induced atrial fibrillation.Cell adhesion & migration · 2026Article
- Disrupting the circTNC/miR-582-5p/MAPK8 axis alleviates oxidative stress-induced trophoblast dysfunction in preeclampsia.Journal of molecular histology · 2026Article
- MicroRNAs in Heart Failure Pathogenesis and Progression: Mechanistic Control, Biomarker Potential, and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
- Dickkopf 2 serves as a novel therapeutic target and prognostic biomarker in acute myeloid leukemia targeted by evodiamine.Frontiers in medicine · 2026Article
- m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling.European journal of medical research · 2025Review
- MicroRNA chemical modifications in post-transcriptional gene silencing and human diseases.Molecular therapy. Nucleic acids · 2025Review
- Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential.Cell biology and toxicology · 2025Review
- METTL3-mediated mActa biochimica et biophysica Sinica · 2025Article
- Exploring m6A modifications in gastric cancer: from molecular mechanisms to clinical applications.European journal of medical research · 2025Review
- Review
- ALKBH5, an m6A demethylase, attenuates tumor growth and inhibits metastasis in papillary thyroid carcinoma.Scientific reports · 2025Article
- Methylations in dilated cardiomyopathy and heart failure.Frontiers in cardiovascular medicine · 2025Review
- METTL3-mediated m6A modification regulates D-galactose-induced skin fibroblast senescence through miR-208a-5p.Frontiers in immunology · 2025Article
- Comprehensive analysis of m6A methylated modification of fibrotic atria in rats induced by chronic intermittent hypoxia.Frontiers in cardiovascular medicine · 2025Article
- Ythdf2 facilitates precursor miR-378/miR-378-5p maturation to support myogenic differentiation.Cellular and molecular life sciences : CMLS · 2024Article
- Epigenetic regulation of cardiovascular diseases induced by behavioral and environmental risk factors: Mechanistic, diagnostic, and therapeutic insights.FASEB bioAdvances · 2024Review
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10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMETTL3 is the core catalytic enzyme in m6A and is involved in a variety of cardiovascular diseases. However, whether and how METTL3 plays a role during angiotensin II (Ang-II)-induced myocardial hypertrophy is still unknown.
methodsNeonatal rat cardiomyocytes (NRCMs) and C57BL/6J mice were treated with Ang-II to induce myocardial hypertrophy. qRT-PCR and western blots were used to detect the expression of RNAs and proteins. Gene function was verified by knockdown and/or overexpression, respectively. Luciferase and RNA immunoprecipitation (RIP) assays were used to verify interactions among multiple genes. Wheat germ agglutinin (WGA), hematoxylin and eosin (H&E), and immunofluorescence were used to examine myocardial size. m6A methylation was detected by a colorimetric kit.
resultsMETTL3 and miR-221/222 expression and m6A levels were significantly increased in response to Ang-II stimulation. Knockdown of METTL3 or miR-221/222 could completely abolish the ability of NRCMs to undergo hypertrophy. The expression of miR-221/222 was positively regulated by METTL3, and the levels of pri-miR-221/222 that bind to DGCR8 or form m6A methylation were promoted by METTL3 in NRCMs. The effect of METTL3 knockdown on hypertrophy was antagonized by miR-221/222 overexpression. Mechanically, Wnt/β-catenin signaling was activated during hypertrophy and restrained by METTL3 or miR-221/222 inhibition. The Wnt/β-catenin antagonist DKK2 was directly targeted by miR-221/222, and the effect of miR-221/222 inhibitor on Wnt/β-catenin was abolished after inhibition of DKK2. Finally, AAV9-mediated cardiac METTL3 knockdown was able to attenuate Ang-II-induced cardiac hypertrophy in mouse model.
conclusionsOur findings suggest that METTL3 positively modulates the pri-miR221/222 maturation process in an m6A-dependent manner and subsequently activates Wnt/β-catenin signaling by inhibiting DKK2, thus promoting Ang-II-induced cardiac hypertrophy. AAV9-mediated cardiac METTL3 knockdown could be a therapeutic for pathological myocardial hypertrophy.
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