ArticleCellular & molecular biology letters2026
NAT10-mediated ac
Article in Cellular & molecular biology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
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Authors and funding
6 authors.
Funding
Abstract
backgroundAcute kidney injury (AKI) is closely linked to inflammatory responses driven by the NF-κB pathway, yet the epigenetic mechanisms underlying this association remain poorly understood. This study investigates the role of N-acetyltransferase 10 (NAT10)-mediated RNA N
methodsClinical AKI specimens and experimental models (in vivo and in vitro) were analyzed to assess NAT10 expression in renal tubular epithelial cells (RTECs). Genetic knockdown and overexpression of NAT10 (including the catalytically inactive NAT10-G641E mutant) were performed in vitro to evaluate NF-κB pathway activity and hypoxia/reoxygenation (H/R)-induced inflammatory responses. In murine ischemia/reperfusion (I/R)-induced AKI models, genetic ablation of NAT10 in RTECs and pharmacological inhibition using Remodelin were employed to study renal inflammation and injury. Mechanistic insights were derived from integrated ac
resultsNAT10 was significantly upregulated in RTECs of clinical AKI specimens and experimental models. In vitro, NAT10 knockdown suppressed NF-κB activation, mitigating H/R-induced inflammation and cellular damage, while NAT10 overexpression (but not the G641E mutant) activated NF-κB, exacerbating RTECs injury. In murine I/R-AKI models, genetic or pharmacological inhibition of NAT10 attenuated NF-κB-mediated renal inflammation and tubular damage. Mechanistically, NAT10-mediated ac
conclusionsThis study identifies the NAT10-ac
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Registered trials
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