ArticlePsychiatry investigation2022
m6A Methyltransferase METTL3 Reduces Hippocampal Neuron Apoptosis in a Mouse Model of Autism Through the MALAT1/SFRP2/Wnt/β-catenin Axis.
Article in Psychiatry investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Unraveling the Role of Wnt Signaling Pathway in the Pathogenesis of Autism Spectrum Disorder (ASD): A Systematic Review.Molecular neurobiology · 2025Pooled it
- Interaction between N6-methyladenosine (mGenes & diseases · 2026Review
- mNature reviews. Neuroscience · 2026Review
- Neuromodulatory role and therapeutic potential of N 6 -methyladenosine RNA methylation in neurodegenerative diseases.Neural regeneration research · 2026Article
- METTL3-mediated mTranslational psychiatry · 2026Article
- Cell death-associated genes as novel diagnostic biomarkers for autism spectrum disorder.Apoptosis : an international journal on programmed cell death · 2026Article
- Neurodevelopmental outcomes relevant to autism in juvenile mice exposed to PCB 11 in the maternal diet throughout gestation and lactation.Frontiers in toxicology · 2026Article
- Differential epigenetic regulation of glucose-induced alteration of miR-9 in retinal and cardiac endothelial cells.PloS one · 2026Article
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- Valproate-Induced Autism and Sexual Hormone Disturbances: A Literature Review and Hypotheses.Neurochemical research · 2025Review
- m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).International journal of molecular medicine · 2025Review
- METTL3-Mediated N6-Methyladenosine Modification Regulates the Progression of Diabetic Retinopathy.Applied biochemistry and biotechnology · 2025Article
- Crosstalk Between N6-Methyladenosine and Other Epigenetic Mechanisms in Central Nervous System Development and Disorders.Biomolecules · 2025Review
- N6-methyladenosine methylation: a novel key to unlocking mental disorders.The international journal of neuropsychopharmacology · 2025Review
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- The Role of Long Non-Coding RNA in Anxiety Disorders: A Literature Review.International journal of molecular sciences · 2025Review
- Therapeutic effects ofFrontiers in pharmacology · 2025Article
- RNA methylation in neurodevelopment and related diseases.Acta biochimica et biophysica Sinica · 2024Review
- N6-Methyladenosine Methylation of mRNA in Cell Apoptosis.Molecular neurobiology · 2024Review
- METTL3 inhibits BMSC apoptosis and facilitates osteonecrosis repair via an m6A-IGF2BP2-dependent mechanism.Heliyon · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveHippocampal neuron apoptosis contributes to autism, while METTL3 has been documented to possess great potentials in neuron apoptosis. Our study probed into the role of METTL3 in neuron apoptosis in autism and to determine the underlying mechanism.
methodsBioinformatics analysis was used to analyze expressed genes in autism samples. Institute of Cancer Research mice were treated with valproic acid to develop autism models. The function of METTL3 in autism-like symptoms in mice was analyzed with behavioral tests and histological examination of their hippocampal tissues. Primary mouse hippocampal neurons were extracted for in vitro studies. Downstream factors of METTL3 were explored and validated.
resultsMETTL3, MALAT1, and Wnt/β-catenin signaling were downregulated, while SFRP2 was upregulated in the hippocampal tissues of a mouse model of autism. METTL3 stabilized MALAT1 expression by promoting m6A modification of MALAT1. MALAT1 promoted SFRP2 methylation and led to reduced SFRP2 expression by recruiting DNMT1, DNMT3A, and DNMT3B to the promoter region of SFRP2. Furthermore, SFRP2 facilitated activation of the Wnt/β-catenin signaling. By this mechanism, METTL3 suppressed autism-like symptoms and hippocampal neuron apoptosis.
conclusionThis research suggests that METTL3 can reduce autism-like symptoms and hippocampal neuron apoptosis by regulating the MALAT1/SFRP2/Wnt/β-catenin axis.
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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.