ArticleScientific reports2025
DNMT3B aggravated renal fibrosis in diabetic kidney disease via activating Wnt/β-catenin signaling pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The lactate-lactylation axis in renal fibrosis: potential mechanisms in diabetic kidney disease.Annals of medicine · 2025Pooled it
- High-Glucose-Induced Metabolic and Epithelial Stress in Grass Carp Intestinal Epithelial Cells Associated with Methylation-Related Transcriptional Responses.International journal of molecular sciences · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Role of the DNA methyltransferases in diabetes mellitus and Its complications.Molecular biology reports · 2026Review
- H19 inhibition orchestrates DNMT3B-dependent epigenetic reprogramming of glycolytic enzymes in the liver during diabetes.Cell communication and signaling : CCS · 2026Article
- An intricate relationship between fibrosis and autoimmune diseases: a specific focus on unraveling its molecular, immunological, and epigenetic drivers.Frontiers in immunology · 2026Review
- Bidirectional regulation between mitochondrial metabolic reprogramming and epigenetic modifications in renal tubular epithelial cell injury of diabetic kidney disease.Frontiers in endocrinology · 2026Review
- Molecular pathways and emerging therapeutic targets in the pathogenesis of diabetic kidney disease.Frontiers in physiology · 2026Review
- Immune-metabolic interactions shape the fibrotic landscape of diabetic kidney disease: emerging mechanisms and therapeutic prospects.Frontiers in physiology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
The incidence of diabetic kidney disease (DKD) has increased rapidly worldwide in recent decades, and DKD is the leading cause of chronic kidney disease. The Wnt/β-catenin pathway is widely recognized as a critical contributor to DKD. However, how this pathway is activated in DKD is still unknown. Recent studies have revealed that epigenetic mechanisms play key roles in DKD. DNA methylation is an epigenetic mechanism that is essential for regulating gene transcription. Here, we demonstrated that reducing the expression of DNMT3B, a DNA methyltransferase, markedly decreased extracellular matrix (ECM) deposition and diabetic renal fibrosis (DRF). Furthermore, we found that DNMT3B activated the Wnt/β-catenin pathway by suppressing SFRP5 expression in HG-induced renal tubular epithelial cells. Mechanistically, we observed that DNMT3B increased the promoter methylation levels of sfrp5, which contributed to a decrease in SFRP5 protein expression. Additionally, Pharmacological disruption of DNA methylation (via 5-Aza) and genetic knockdown of DNMT3B suppressed the Wnt/β-catenin pathway, leading to the attenuation of ECM deposition and DRF. Thus, our study provides a novel understanding of the epigenetic regulation of DKD pathogenesis and a new therapeutic strategy for DKD by disrupting the Wnt/β-catenin pathway.
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