ArticleJournal of the American Society of Nephrology : JASN2024
METTL3-Mediated N 6 -Methyladenosine mRNA Modification and cGAS-STING Pathway Activity in Kidney Fibrosis.
Article in Journal of the American Society of Nephrology : JASN, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Cell-Specific Roles of Angiopoietin-2 in CKD.Journal of the American Society of Nephrology : JASN · 2026Article
- RNA mActa pharmacologica Sinica · 2026Review
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- METTL14 Downregulation Accelerates HBV-Related Cirrhosis and Hepatocellular Carcinoma by Promoting Type I Interferon Release via the cGAS-STING Pathway Through mJournal of medical virology · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Epitranscriptomics in kidney disease: insights and therapeutic potential.Kidney research and clinical practice · 2026Article
- m6A-Mediated epitranscriptional reprogramming drives cardiac fibrosis by suppressing PGC-1α and boosting mitochondrial fission.Journal of translational medicine · 2026Article
- The epigenetic and epitranscriptomic regulation of Brd4-Mettl3 axis on STING mediated vascular calcification.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Emerging Mechanistic Roles of STING Signaling in Kidney Diseases.The American journal of pathology · 2026Review
- Energy-sensing molecule RORγ regulates cholesterol metabolism and immune signaling in diabetic kidney disease and aging.Nature communications · 2026Article
- Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.Frontiers in pharmacology · 2026Review
- Role of the cGAS-STING signaling pathway in diabetes mellitus and its complications: from mechanisms to therapeutics.Frontiers in pharmacology · 2026Review
- The dual role of the cGAS-STING signaling pathway in kidney diseases: from acute injury to chronic fibrosis - molecular mechanisms and precision therapeutic strategies.Frontiers in pharmacology · 2026Review
- ADSC-derived exosomes inhibit myofibroblast transdifferentiation and attenuate airway stenosis via METTL3-mediated m6A modification of TLR2.American journal of translational research · 2026Article
- Bimodal regulation and precision therapy of neutrophil extracellular traps in liver ischemia-reperfusion injury: recent advances.Frontiers in immunology · 2026Review
- Emerging epigenetic modifications in renal fibrosis: From mechanisms to treatments.Acta pharmaceutica Sinica. B · 2025Review
- Breaking barriers: The cGAS-STING pathway as a novel frontier in cancer immunotherapy.Cancer communications (London, England) · 2025Review
- Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Review
- STING inhibition alleviates experimental peritoneal damage: potential therapeutic relevance for peritoneal dialysis.The Journal of pathology · 2025Article
- METTL3-mediated mMolecular biology reports · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Background: Chemical modifications on RNA profoundly affect RNA function and regulation. m6A, the most abundant RNA modification in eukaryotes, plays a pivotal role in diverse cellular processes and disease mechanisms. However, its importance is understudied in human CKD samples regarding its influence on pathological mechanisms. Methods: Liquid chromatography–tandem mass spectrometry and methylated RNA immunoprecipitation sequencing were used to examine alterations in m6A levels and patterns in CKD samples. Overexpression of the m6A writer METTL3 in cultured kidney tubular cells was performed to confirm the effect of m6A in tubular cells and explore the biological functions of m6A modification on target genes. In addition, tubule-specific deletion of Mettl3 (Ksp-Cre Mettl3f/f) mice and antisense oligonucleotides inhibiting Mettl3 expression were used to reduce m6A modification in an animal kidney disease model. Results: By examining 127 human CKD samples, we observed a significant increase in m6A modification and METTL3 expression in diseased kidneys. Epitranscriptomic analysis unveiled an enrichment of m6A modifications in transcripts associated with the activation of inflammatory signaling pathways, particularly the cyclic guanosine monophosphate–AMP synthase (cGAS)-stimulator of IFN genes (STING) pathway. m6A hypermethylation increased mRNA stability in cGAS and STING1 as well as elevated the expression of key proteins within the cGAS-STING pathway. Both the tubule-specific deletion of Mettl3 and the use of antisense oligonucleotides to inhibit Mettl3 expression protected mice from inflammation, reduced cytokine expression, decreased immune cell recruitment, and attenuated kidney fibrosis. Conclusions: Our research revealed heightened METTL3-mediated m6A modification in fibrotic kidneys, particularly enriching the cGAS-STING pathway. This hypermethylation increased mRNA stability for cGAS and STING1, leading to sterile inflammation and fibrosis.
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