ArticleBMC nephrology2022
METTL3 enhances NSD2 mRNA stability to reduce renal impairment and interstitial fibrosis in mice with diabetic nephropathy.
Article in BMC nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- 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 N6-Methyladenosine Modification Regulates the Progression of Diabetic Retinopathy.Applied biochemistry and biotechnology · 2025Article
- The UBR5 protein facilitates mesangial cell hypertrophy and glycolysis induced by high glucose by increasing the phosphorylation levels of AKT.Acta diabetologica · 2025Article
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- METTL3 Potentiates M2 Macrophage-Driven MMT to Aggravate Renal Allograft Fibrosis via the TGF-β1/Smad3 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- m6A Ribonucleic Acid Methylation in Fibrotic Diseases of Visceral Organs.Small science · 2025Review
- m6A RNA modification pathway: orchestrating fibrotic mechanisms across multiple organs.Briefings in functional genomics · 2025Review
- The latest progression of N6-methyladenosine (mFrontiers in endocrinology · 2025Review
- KLF7 reverses ox-LDL-induced ferroptosis in HMEC-1 cells through transcriptionally activating ALKBH5 to inhibit the m6A modification of ACSL4.Cytotechnology · 2024Article
- Methyltransferase-like 3 represents a prospective target for the diagnosis and treatment of kidney diseases.Human genomics · 2024Review
- N6-methyladenosine (m6A) RNA modification in fibrosis and collagen-related diseases.Clinical epigenetics · 2024Review
- Nucleic acid and protein methylation modification in renal diseases.Acta pharmacologica Sinica · 2024Review
- Article
- N6-methyladenine RNA methylation epigenetic modification and diabetic microvascular complications.Frontiers in endocrinology · 2024Review
- Targeting METTL3 enhances the chemosensitivity of non-small cell lung cancer cells by decreasing ABCC2 expression in an mInternational journal of biological sciences · 2024Article
- The role of N-methyladenosine modification in acute and chronic kidney diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- N6-methyladenosine methylation in kidney injury.Clinical epigenetics · 2023Review
- Intron retention decreases METTL3 expression by inhibiting mRNA export to the cytoplasm.BMB reports · 2023Article
- Multilevel regulation of NGenes & diseases · 2023Review
- The role of mFrontiers in endocrinology · 2023Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNuclear receptor-binding SET domain protein 2 (NSD2) is a histone methyltransferase that has been demonstrated to regulate insulin secretion and glucose concentration. This study focused on the role of NSD2 in the renal impairment during diabetic nephropathy (DN).
methodsSerum NSD2 level in patients with DN was examined, and its correlations with the renal impairment-related indicators were examined. A murine model of DN was established, and mouse mesangial cells (SV40-MES-13) were treated with high-glucose (HG) to mimic a DN-like condition in vitro. Overexpression of NSD2 was introduced into mice or cells for in vivo and in vitro studies. The m6A level in HG-treated SV40-MES-13 cells was analyzed. METTL3 expression and its correlation with NSD2 were determined.
resultsNSD2 was poorly expressed in the serum of patients with DN and was negatively correlated with the levels of fasting blood sugar (FBG), serum creatinine (SCr), serum cystatin C (S-Cys-C), the 24-h urine protein (24-h U-protein) and the urine cystatin C (U-Cys-C). NSD2 overexpression reduced the kidney weight and reduced renal impairment in mice. It also suppressed interstitial fibrosis in mouse kidney tissues and reduced fibrosis-related markers in HG-treated SV40-MES-13 cells. HG treatment reduced the m6A level in the cells. METTL3 promoted m6A modification of NDS2 mRNA and enhanced its stability by YTHDF1. METTL3 overexpression alleviated renal impairment and fibrosis in vivo and in vitro. But the protective role was blocked upon NSD2 silencing.
conclusionThis study demonstrates that METTL3 promotes NSD2 mRNA stability by YTHDF1 to alleviate progression of DN.
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