ArticleJournal of molecular cell biology2023
METTL3-mediated m6A modification of HMGA2 mRNA promotes subretinal fibrosis and epithelial-mesenchymal transition.
Article in Journal of molecular cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Regulatory mechanisms and therapeutic potential of N6-methyladenosine modification in retinal diseases (Review).Molecular medicine reports · 2026Review
- SPI1 Promotes TNF-α-Induced Epithelial-Mesenchymal Transition-Like Changes in Retinal Pigment Epithelial Cells: Implications for the Pathogenesis of Age-Related Macular Degeneration.Journal of ophthalmology · 2026Article
- Cepharanthine inhibits the proliferation and epithelial-mesenchymal transition of oral squamous cell carcinoma via HMGA2/FOXL2 axis.BMC pharmacology & toxicology · 2025Article
- MicroRNA let-7a mitigates the progression of oral submucous fibrosis by targeting high-mobility group AT-hook 2.Journal of dental sciences · 2025Article
- RNA 5-Methylcytosine Modification in Myocardial Fibrosis.Reviews in cardiovascular medicine · 2025Review
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Molecular Mechanisms of Epithelial-Mesenchymal Transition in Retinal Pigment Epithelial Cells: Implications for Age-Related Macular Degeneration (AMD) Progression.Biomolecules · 2025Review
- m6A RNA modification pathway: orchestrating fibrotic mechanisms across multiple organs.Briefings in functional genomics · 2025Review
- Intracellular Signaling Pathways and Their Potential Targeting for Treatment of Ocular Posterior Segment Fibrosis.Journal of ophthalmic & vision research · 2025Review
- METTL3 blocked the progression of diabetic retinopathy through m6A-modified SOX2.Open medicine (Warsaw, Poland) · 2025Article
- Integration of multi-omics data reveals dysregulated RNA methylation in retinal pigment epithelium drives age-related macular degeneration.International journal of ophthalmology · 2025Article
- Inhibition of HPSE/SDC-2 axis-induced epithelial-mesenchymal transition for treating IC/BPS.PloS one · 2025Article
- Silencing METTL3 Increases HSP70 Expression and Alleviates Fibrosis in Keratocytes.Investigative ophthalmology & visual science · 2024Article
- METTL3-mediated m6A modification of SIRT1 mRNA affects the progression of diabetic cataracts through cellular autophagy and senescence.Journal of translational medicine · 2024Article
- N6-methyladenosine (m6A) RNA modification in fibrosis and collagen-related diseases.Clinical epigenetics · 2024Review
- Examining the evidence for mutual modulation between m6A modification and circular RNAs: current knowledge and future prospects.Journal of experimental & clinical cancer research : CR · 2024Review
- m6A-Mediated Upregulation of Imprinted in Prader-Willi Syndrome Induces Aberrant Apical-Basal Polarization and Oxidative Damage in RPE Cells.Investigative ophthalmology & visual science · 2024Article
- WTAP-mediated N6-methyladenosine mRNA methylation regulates laser-induced macular neovascularization.Molecular vision · 2024Article
- Comprehensive Transcriptomic Profiling of m6A Modification in Age-Related Hearing Loss.Biomolecules · 2023Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subretinal fibrosis is a major cause of the poor visual prognosis for patients with neovascular age-related macular degeneration (nAMD). Myofibroblasts originated from retinal pigment epithelial (RPE) cells through epithelial-mesenchymal transition (EMT) contribute to the fibrosis formation. N6-Methyladenosine (m6A) modification has been implicated in the EMT process and multiple fibrotic diseases. The role of m6A modification in EMT-related subretinal fibrosis has not yet been elucidated. In this study, we found that during subretinal fibrosis in the mouse model of laser-induced choroidal neovascularization, METTL3 was upregulated in RPE cells. Through m6A epitranscriptomic microarray and further verification, high-mobility group AT-hook 2 (HMGA2) was identified as the key downstream target of METTL3, subsequently activating potent EMT-inducing transcription factor SNAIL. Finally, by subretinal injections of adeno-associated virus vectors, we confirmed that METTL3 deficiency in RPE cells could efficiently attenuate subretinal fibrosis in vivo. In conclusion, our present research identified an epigenetic mechanism of METTL3-m6A-HMGA2 in subretinal fibrosis and EMT of RPE cells, providing a novel therapeutic target for subretinal fibrosis secondary to nAMD.
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