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Epitranscriptomics in kidney disease: insights and therapeutic potential
Yu-Cheng Tsai1, Ming-Tsun Tsai1,2, Shuo-Ming Ou1,2
1Division of Nephrology, Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Kidney Research and Clinical Practice
|May 15, 2026
Summary
N6-methyladenosine (m⁶A) RNA methylation is crucial in kidney disease by affecting gene expression. Targeting m⁶A pathways offers new therapeutic strategies for renal fibrosis and other kidney conditions.
Area of Science:
- Molecular Biology
- Genetics
- Nephrology
Background:
- Epitranscriptomic regulation, specifically N6-methyladenosine (m⁶A) RNA methylation, is a key mechanism controlling gene expression.
- m⁶A is the most abundant internal modification in eukaryotic mRNA, influencing splicing, stability, translation, and localization via specific proteins.
- Recent research highlights the significant involvement of m⁶A in the pathogenesis of kidney diseases and renal fibrosis.
Purpose of the Study:
- To review the current understanding of m⁶A-mediated gene regulation in kidney disease.
- To elucidate the mechanistic insights and disease-specific alterations related to m⁶A in renal pathophysiology.
- To explore emerging therapeutic strategies targeting m⁶A pathways for kidney disorders.
Main Methods:
- Literature review synthesizing current knowledge on m⁶A in kidney disease.
- Analysis of m⁶A machinery's role in pathogenic pathways.
- Examination of m⁶A-modified noncoding RNAs in fibrogenic and immune networks.
Main Results:
- Dysregulation of the m⁶A epitranscriptomic system impacts critical pathways in kidney disease development.
- m⁶A modifications in noncoding RNAs integrate into fibrotic and immune regulatory processes.
- Targeting m⁶A pathways shows therapeutic potential, with ongoing development of inhibitors and editing technologies.
Conclusions:
- m⁶A epitranscriptomics plays a vital role in kidney disease pathogenesis and progression.
- Targeting m⁶A offers promising therapeutic avenues for renal fibrosis and other kidney diseases.
- Further research into tissue-specific modulation and toxicity is needed for effective m⁶A-based therapies.
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