Epigenetic Regulatory Mechanisms and Therapeutic Potential of DNMT1 in Kidney Diseases

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Epigenetic Regulatory Mechanisms and Therapeutic Potential of DNMT1 in Kidney Diseases

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Co-author 1

Xiaofei Huang 13062635420@163.com Shanghai general hosiptal Department of Nephrology Shanghai China *

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Nan Zhu znnancy@yeah.net Shanghai general hosiptal Department of Nephrology Shanghai China -

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Introduction

DNA methyltransferase 1 (DNMT1), a key enzyme responsible for maintaining DNA methylation patterns, contributes to the progression of kidney diseases through epigenetic regulation of gene expression. Emerging evidence highlights aberrant DNMT1 expression in diabetic kidney disease (DKD), hepatitis B virus-associated glomerulonephritis (HBV-GN), acute kidney injury (AKI), chronic kidney disease (CKD), autosomal dominant polycystic kidney disease (ADPKD),and clear cell renal cell carcinoma (ccRCC). However, the multidimensional regulatory mechanisms and therapeutic targeting strategies of DNMT1 in renal pathologies remain to be systematically elucidated.

Methods

This study comprehensively dissects the pivotal roles of DNMT1 in kidney diseases:

Inflammation and Fibrosis: DNMT1 induces hypermethylation of the SOCS1 promoter, suppressing its expression and activating the JAK2/STAT3 pathway to exacerbate inflammatory responses in DKD. Concurrently, DNMT1-mediated Klotho gene methylation silences its expression, activating the β-catenin/Snail axis to drive renal tubular epithelial-mesenchymal transition (EMT) and fibrosis.

Podocyte Injury: Under hyperglycemic conditions, DNMT1 overexpression downregulates slit diaphragm proteins (nephrin, podocin) and triggers podocyte apoptosis via the FOXF1/miR-342-3p/E2F1 signaling axis.

Oncogenesis and Genetic Disorders: In ccRCC, DNMT1 epigenetically silences hepaCAM, thereby activating the PI3K/Akt pathway to promote tumor progression. In ADPKD, DNMT1 amplifies cystogenesis by enhancing PTPRM/PTPN22 methylation through the STAT3 feedback loop.

Results

Therapeutic Implications: DNMT1 inhibitors (e.g., Rhein, epigallocatechin gallate [EGCG]) ameliorate aberrant DNA methylation, attenuating inflammation, fibrosis, and podocyte injury in preclinical models. However, challenges persist regarding suboptimal target specificity and potential risks of genomic instability.

Conclusion

DNMT1 orchestrates epigenetic dysregulation in diverse kidney pathologies, including inflammation, fibrosis, and abnormal cellular proliferation, positioning it as a promising therapeutic target. Nevertheless, clinical translation of DNMT1 inhibitors necessitates resolution of tissue-specific delivery and long-term safety concerns. This study provides novel insights into molecular mechanisms and precision medicine strategies for kidney diseases.

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