ArticleCell death discovery2023
N-acetyltransferase 10 promotes cutaneous wound repair via the NF-κB-IL-6 axis.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 11 citations in OpenAlex.
- Treatment with dapagliflozin and empagliflozin reduces concentrations of N4-acetylcytidine in plasma, a biomarker associated with vascular damage.Cardiovascular diabetology · 2026Article
- NAT10-mediated acCellular & molecular biology letters · 2026Article
- The NAT10/acCell communication and signaling : CCS · 2026Review
- RNA modifications: molecular orchestrators of wound healing.Burns & trauma · 2026Article
- Cellular and Molecular Mechanisms of Wound Repair: From Biology to Therapeutic Innovation.Cells · 2025Review
- NAT10 Mediates Cardiac Fibrosis Induced by Myocardial Infarction Through ac4C Modification of TGFBR1 mRNA.Cell biology and toxicology · 2025Article
- Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.Molecular biomedicine · 2025Review
- Single-cell imaging of N4-acetylcytidine-modified RNA using fluorine metabolic labeling mediated proximity ligation assay.Nucleic acids research · 2025Article
- Bridging tissue repair and epithelial carcinogenesis: epigenetic memory and field cancerization.Cell death and differentiation · 2025Review
- Critical Analysis of Cytoplasmic Progression of Inflammatory Signaling Suggests Potential Pharmacologic Targets for Wound Healing and Fibrotic Disorders.Biomedicines · 2024Review
- NAT10 and cytidine acetylation in mRNA: intersecting paths in development and disease.Current opinion in genetics & development · 2024Review
- ac4C: a fragile modification with stabilizing functions in RNA metabolism.RNA (New York, N.Y.) · 2024Review
- Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cutaneous wound healing, an integral part for protection of skin barrier, is a complex biological process and intimately associated with keratinocyte migration. However, mechanisms regulating keratinocyte migration in the process of cutaneous wound repair remain largely unknown. Here, we found that N-acetyltransferase 10 (NAT10) is essential for cutaneous wound repair in an in vivo skin wound healing model-a significant delay of wound repair in Nat10 haploinsufficient mice and a remarkable inhibition of keratinocyte migration by NAT10 knockdown in an in vitro keratinocyte migration model. We further demonstrate that loss of NAT10 expression attenuates the wound-induced IL-6/IL-8 expression through inhibiting NF-κB/p65 activity in keratinocytes. By deeply digging, silencing NAT10 compromises the level of nuclear p65 by facilitating its poly-ubiquitination, thus accelerates its degradation in the nucleus. Notably, we detected a strong positive correlation between the expression of NAT10 and relevant NF-kB/p65-IL6 signaling activity in mouse wound skin tissues. Overall, our study reveals an important role of NAT10 on cutaneous wound repair by potentiating NF-κB/p65-IL-6/8-STAT3 signaling. Targeting NAT10 might be a potential strategy for the treatment of skin wound dysfunctions and related diseases.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.