ArticleJournal of diabetes investigation2024
METTL3/YTHDF2 m6A axis mediates the progression of diabetic nephropathy through epigenetically suppressing PINK1 and mitophagy.
Article in Journal of diabetes investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- The Role of NMedComm · 2026Review
- mRedox biology · 2026Review
- YTH Domain Family 2 Promotes Tubal Factor Infertility through Reducing H3K4me1 Methylation of CYLD by KMT2D.Applied biochemistry and biotechnology · 2026Article
- METTL14/IGF2BP1 mInfection and immunity · 2026Article
- The translational potential of m6A RNA methylation in DKD: emerging biomarkers for early detection and targeted therapies.Frontiers in medicine · 2026Review
- Astragalus polysaccharide alleviates diabetic nephropathy via SIRT1-dependent activation of FOXO3a/BNIP3 pathway to enhance podocyte autophagy.Scientific reports · 2025Article
- METTL3 promotes podocyte pyroptosis in diabetic nephropathy through NRenal failure · 2025Article
- METTL3 alleviates renal tubular mitochondrial dysfunction by regulating the TUG1/PGC-1a axis in an IGF2BP2-dependent manner in diabetic nephropathy.Renal failure · 2025Article
- METTL3-mediated mMolecular biology reports · 2025Review
- METTL3/YTHDF3 mJournal of diabetes investigation · 2025Article
- RNA Modification in Metabolism.MedComm · 2025Review
- MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mitochondria and myocardial ischemia/reperfusion injury: Effects of Chinese herbal medicine and the underlying mechanisms.Journal of pharmaceutical analysis · 2025Review
- m6A Ribonucleic Acid Methylation in Fibrotic Diseases of Visceral Organs.Small science · 2025Review
- Landscape analysis of m6A modification regulators reveals LRPPRC as a key modulator in tubule cells for DKD: a multi-omics study.Frontiers in pharmacology · 2025Article
- METTL3-driven mFrontiers in immunology · 2025Article
- The latest progression of N6-methyladenosine (mFrontiers in endocrinology · 2025Review
- circARID1A Inhibits Tail Fat Cell Differentiation in Guangling Large-Tailed Sheep by Regulating the miR-493-3p/YTHDF2 Axis.International journal of molecular sciences · 2024Article
- Methyltransferase-like 3 represents a prospective target for the diagnosis and treatment of kidney diseases.Human genomics · 2024Review
- N6-methyladenine RNA methylation epigenetic modification and diabetic microvascular complications.Frontiers in endocrinology · 2024Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
aimsThis research aimed to investigate the specific mechanism of methyltransferase like 3 (METTL3) in the progression of diabetic kidney disease (DKD). MATERIALS AND
methodsThe model of diabetic kidney disease was established with HK-2 cells and mice in vitro and in vivo. The N6 methyladenosine (m6A) contents in the cells and tissues were detected with a commercial kit and the m6A levels of PTEN induced putative kinase 1 (PINK2) were detected with a MeRIP kit. The mRNA and protein levels were determined with RT-qPCR and western blot. The ROS, TNF-α, and IL-6 levels were assessed with ELISA. The cell proliferative ability was measured by a CCK-8 assay and cell apoptosis was determined with TUNEL staining. The HE and Masson staining was performed to observe the renal morphology. The RIP assay was conducted to detect the interaction between METTL3/YTHDF2 and PINK1.
resultsThe m6A content and METTL3 levels were prominently elevated in diabetic kidney disease. METTL3 silencing promoted the cell growth and the expression of LC3 II, PINK1, and Parkin, while inhibiting the cell apoptosis and the expression of LC3 I and p62 in the high glucose (HG) stimulated HK-2 cells. METTL3 silencing also decreased the ROS, TNF-α, and IL-6 levels in diabetic kidney disease. PINK1 silencing neutralized the function of sh-METTL3 in the HG stimulated HK-2 cells. The HE and Masson staining showed that METTL3 silencing alleviated the kidney injury induced by DKD. METTL3 silencing decreased the m6A levels of PINK1, while increased the mRNA levels of PINK1 which depended on YTHDF2.
conclusionsMETTL3 silencing could inhibit the progression of diabetic nephropathy in vivo and in vitro by regulating the m6A modification of PINK1, which depends on YTHDF2. Our research lays the theoretical foundation for the precise treatment of diabetic kidney disease and the development of targeted drugs in the future.
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