ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
METTL3 Potentiates M2 Macrophage-Driven MMT to Aggravate Renal Allograft Fibrosis via the TGF-β1/Smad3 Pathway.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Article
- PI3K/AKT signaling pathway: molecular crossroads in tumorigenesis and therapeutic innovation.Signal transduction and targeted therapy · 2026Review
- MMT: A Potential Mechanism of Myocardial Fibrosis - Regulation of the TGF-β1/Smad3 Pathway and Prospects for Targeted Therapy.Reviews in cardiovascular medicine · 2026Review
- SPP1+ macrophages contribute to silica-induced pulmonary inflammation and fibrosis via the ERK/JNK signaling pathway.American journal of respiratory cell and molecular biology · 2026Article
- Article
- Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil.iScience · 2026Article
- Curcumin Inhibits Renal Fibrosis by Suppressing S100A8/A9-TLR4 Signaling via Gut Microbiota-Derived Short-Chain Fatty Acid in Macrophages.Molecular nutrition & food research · 2026Article
- Epitranscriptomic silencing of the ZC3H13/mJournal of experimental & clinical cancer research : CR · 2026Article
- ASCL2-mediated macrophage-myofibroblast transition generates immunosuppressive CAF_7 in NSCLC bone metastases.Journal of experimental & clinical cancer research : CR · 2026Article
- Hdac11 promotes idiopathic pulmonary fibrosis through macrophage M2-type polarization and myofibroblast accumulation by inhibiting Parkin-dependent mitophagy.Nature communications · 2026Article
- Targeting lactylation in a novel metabolic-epigenetic-inflammatory axis mitigates inflammation and promotes healing following corneal injury.Journal of translational medicine · 2026Article
- METTL3 Potentiates Corneal Allograft Rejection via Increased Pro-Inflammatory Cytokine Production and Aerobic Glycolysis.Investigative ophthalmology & visual science · 2026Article
- Rubiadin-1-methyl ether alleviates bleomycin induced pulmonary fibrosis.Scientific reports · 2026Article
- Dapagliflozin attenuates diabetic renal fibrosis by inhibiting macrophage-myofibroblast transitionPeerJ · 2026Article
- Haikun Shenxi Capsule Alleviates Renal Fibrosis in CKD Mice by Targeting the METTL3/IGF2BP3-Mediated m6A Modification of NKD2.Mediators of inflammation · 2026Article
- Macrophage metabolic reprogramming in organ transplantation: mechanisms, transplant outcomes, and therapeutic implications.Frontiers in cellular and infection microbiology · 2026Review
- The emerging role of mFrontiers in immunology · 2026Review
- Bone Marrow-Derived Macrophage NLRP3 Mediates Renal Fibrosis by triggering TGF-β/Smad3-mediated Macrophage-Myofibroblast Transition.International journal of biological sciences · 2026Article
- Whitlockite-loaded silk fibroin/polyvinyl alcohol hydrogel composited with porous tantalum scaffold enhances bone regeneration and immunomodulation via the TGF-β/NRROS signaling pathway.Materials today. Bio · 2025Article
- Emerging epigenetic modifications in renal fibrosis: From mechanisms to treatments.Acta pharmaceutica Sinica. B · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
METTL3, a key enzyme in N6-methyladenosine (m6A) modification, plays a crucial role in the progression of renal fibrosis, particularly in chronic active renal allograft rejection (CAR). This study explored the mechanisms by which METTL3 promotes renal allograft fibrosis, focusing on its role in the macrophage-to-myofibroblast transition (MMT). Using a comprehensive experimental approach, including TGF-β1-induced MMT cell models, METTL3 conditional knockout (METTL3 KO) mice, and renal biopsy samples from patients with CAR, the study investigates the involvement of METTL3/Smad3 axis in driving MMT and renal fibrosis during the episodes of CAR. We found that elevated m6A modification and METTL3 levels strongly correlated with enhanced MMT and increased fibrotic severity. METTL3 knockout (METTL3 KO) significantly increased the m6A modification of Smad3, decreased Smad3 expression, and inhibited M2-driven MMT. Smad3 knockdown with siRNA (siSmad3) further inhibited M2-driven MMT, while Smad3 overexpression rescued the inhibitory effects of METTL3 silencing, restoring M2-driven MMT and fibrotic tissue damage. Additionally, the METTL3 inhibitor STM2457 effectively reversed M2-driven MMT and alleviated fibrotic tissue damage in CAR. These findings highlight that METTL3 enhances M2-driven MMT in renal fibrosis during CAR by promoting the TGF-β1/Smad3 axis, suggesting that METTL3 is a promising therapeutic target for mitigating renal fibrosis in CAR.
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