Evidence map›Paper›PMID 42633271›Full record

ArticleJournal of pharmaceutical analysis2026

NAT10 aggravates psoriasis by promoting keratinocytes fatty acid synthesis via stable FASN transcription.

Weibo Tang, Jingling Shen, Jiaxin Liu, Chunhui Jiang, Wenya Liu, Mengyao Xiao, Jindan Dai, Wenjie Gao, Junjie Lu, Chunyi Hu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of pharmaceutical analysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Weibo TangState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Jingling ShenInstitute of Life Sciences, College of Life and Environmental Sciences, Wenzhou University, Wenzhou, Zhejiang, 325000, China.
Jiaxin LiuTranslational Medicine Laboratory, Jilin Medical University, Jilin, Jilin, 132013, China.
Chunhui JiangState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Wenya LiuState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Mengyao XiaoState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Jindan DaiState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Wenjie GaoState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Junjie LuState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Chunyi HuState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Yonghuan SongDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China.
Ye XuTranslational Medicine Laboratory, Jilin Medical University, Jilin, Jilin, 132013, China.
Zhongxin ZhuState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Weitao CongState Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNA modifications have emerged as critical regulators of cellular function and disease pathogenesis; however, their contribution to psoriasis remains unclear. Here, we report that N-acetyltransferase 10 (NAT10) expression is markedly elevated in the epidermis of patients with psoriasis and in imiquimod (IMQ)-induced lesions. Single-cell RNA sequencing further identifies NAT10 upregulation in hyperproliferative and basal keratinocyte subsets. Keratinocyte-specific deletion of NAT10 attenuates IMQ-induced psoriatic phenotypes in mice. Integrative profiling of RNA sequencing and N4-acetylcytidine (ac4C) immunoprecipitation sequencing reveals fatty acid synthase (FASN) as a direct downstream target of NAT10. Mechanistically, NAT10 catalyzes ac4C RNA modification to enhance the stability of FASN mRNA, thereby driving fatty acid metabolic reprogramming and promoting keratinocyte proliferation. This metabolic shift contributes to epidermal hyperplasia and inflammation in psoriasis. Notably, pharmacological inhibition of NAT10 with remodelin alleviates disease severity

Indexed as

ac4C modificationFatty acid synthaseNAT10ProliferationPsoriasis

Identifiers

PMID42633271
PMCPMC13499481

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.