ArticleLipids in health and disease2024
NAT10 promotes liver lipogenesis in mouse through N4-acetylcytidine modification of Srebf1 and Scap mRNA.
Article in Lipids in health and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- Depletion of NAT10 in T cells attenuates metabolic dysfunction-associated steatohepatitis in mice.Hepatology communications · 2026Article
- TRIM28-mediated SUMOylation of SREBF1 drives PD‑L1 N‑glycosylation and immune evasion in bladder cancer.Cell death & disease · 2026Article
- Review
- The NAT10/acCell communication and signaling : CCS · 2026Review
- A Global Perspective on Metabolic Dysfunction-Associated Steatotic Liver Disease: From Molecular Mechanisms to Therapeutic Strategy Innovation.Nutrients · 2026Review
- NAT10 and ac4C modification in cancer immunity and metabolism: emerging mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- Epitranscriptomic modifications in programmed cell death: mechanistic insights and implications for liver diseases.Cellular & molecular biology letters · 2025Review
- NAT10-mediated N4-acetylcytidine modification in KLF9 mRNA promotes adipogenesis.Cell death and differentiation · 2025Article
- Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.Molecular biomedicine · 2025Review
- N-acetyltransferase 10 regulates UNC-51-like kinase 1 to reduce tubular cell injury and kidney stone formation.CytoJournal · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundMetabolic dysfunction associated steatotic liver disease (MASLD), closely linked to excessive lipogenesis, induces chronic liver disease. MASLD often cause other metabolic diseases, such as cardiovascular disease, diabetes and obesity. However, the mechanism of N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) mRNA modification in lipogenesis of MASLD has not been fully elucidated. This study investigated the role of NAT10 in lipogenesis targeting mRNA ac4C modification.
methodsThe expression of NAT10 in mouse liver was assessed after a 12-week high-fat diet. In addition, the expression of NAT10 also was detected after AML12 hepatocytes cells were treated with 150 µmol/L palmitic acid (PA). The ac4C mRNA modification was performed by dot blotting. Oil red O staining and the mRNA expression of Srebf1, Acaca and Fasn were used to assess lipogenesis in AML12 cells with NAT10 overexpression or knockdown. acRIP-PCR and NAT10 RIP-PCR were used to verify the Srebf1 and Scap mRNA ac4C modification by NAT10. Furthermore, the liver lipogenesis was evaluated by AAV-mediated target knockdown of NAT10 in mouse liver and treating a specific inhibitor, Remodelin.
resultsThis study revealed that NAT10 is significantly upregulated in liver lipogenesis after a 12-week high-fat diet. NAT10 and ac4C mRNA modification were also drastically increased in AML12 cells after treated with 150 µmol/L PA. Silencing of NAT10 notably inhibited the lipogenesis in AML12 cells and AAV-mediated target knockdown of NAT10 in mouse liver. The acRIP-PCR and NAT10-RIP-PCR revealed that NAT10 ac4C modified Srebf1 and Scap mRNA, the critical modulator of liver lipogenesis, to regulate liver lipogenesis. Besides, Remodelin strongly inhibited liver lipogenesis, including liver TG, serum ALT, AST, TG and TC level and glucose metabolism.
conclusionsNAT10 mediates ac4C modification of Srebf1 and Scap mRNA, thereby affecting lipogenesis in the liver. This study provided a new target for the treatment of MASLD.
Indexed as
Identifiers
What OpenQuestion holds
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.