ArticleCytoJournal2024
N-acetyltransferase 10 regulates UNC-51-like kinase 1 to reduce tubular cell injury and kidney stone formation.
Article in CytoJournal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Regulated Cell Death in Calcium Oxalate Stone Disease: From Tubular Epithelial Injury to Inflammatory Amplification.Journal of inflammation research · 2026Review
- Clinical features ofFrontiers in cellular and infection microbiology · 2026Article
- NAT10 Promotes Tubular Epithelial Cell Senescence in Cisplatin-Induced Acute Kidney Injury by Regulating DDX17.International journal of biological sciences · 2026Article
- Epitranscriptomic modifications in programmed cell death: mechanistic insights and implications for liver diseases.Cellular & molecular biology letters · 2025Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Among the most common chronic kidney diseases, kidney stones are second only to hypertension. Kidney stones pose a public health threat due to their increased incidence, high recurrence rate, and heavy economic burden. In this work, we investigated the potential mechanism of N-acetyltransferase 10 (NAT10) in oxidative stress and pyroptosis of renal tubular epithelial cells (RTECs). Material and Methods: A kidney-stone cell model was simulated using calcium oxalate monohydrate (COM) Results: COM can dose-dependently suppressed the cell viability and superoxide dismutase activity of HK-2 cells and promoted the release of lactate dehydrogenase and malondialdehyde levels ( Conclusion: This study confirmed that NAT10 inhibits RTECs oxidative stress and cell pyrodeath through the enhanced ac4C modification of ULK1 and impedes kidney stone progression.
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