Evidence map›Paper›PMID 38312597›Full record

ArticleHeliyon2024

NAT10 promotes renal ischemia-reperfusion injury via activating NCOA4-mediated ferroptosis.

Jie Shen, Yangyang Sun, Qianfeng Zhuang, Dong Xue, Xiaozhou He

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
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

15 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. NAT10-mediated acCellular & molecular biology letters · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Review
  13. Review
  14. Review
  15. NAT10-mediated acMolecular medicine (Cambridge, Mass.) · 2024
    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

5 authors at 1 institution in 1 country.

Jie ShenDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Yangyang SunDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Qianfeng ZhuangDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Dong XueDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Xiaozhou HeDepartment of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, People's Republic of China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion injury (IRI) is a significant contributor to acute kidney injury (AKI) and is associated with substantial morbidity and mortality rates. In this study, we aimed to investigate the role of NAT10 and its ac4C RNA modification in IRI-induced renal injury. Our findings revealed that both the expression level of NAT10 and the RNA ac4C level in the kidneys were elevated in the IRI group compared to the sham group. Functionally, we observed that inhibition of NAT10 activity with Remodelin or the specific knockout of NAT10 in the kidney led to a significant attenuation of IRI-induced renal injury. Furthermore, in vitro experiments demonstrated that NAT10 inhibition and specific knockout of NAT10 in the kidney markedly suppressed global ac4C RNA modification, providing protection against hypoxia/reoxygenation-induced tubular epithelial cell injury and ferroptosis. Mechanistically, our study uncovered that NAT10 promoted ac4C RNA modification of NCOA4 mRNA, thereby enhancing its stability and contributing to IRI-induced ferroptosis in tubular epithelial cells (TECs). These findings underscore the potential of NAT10 and ac4C RNA modification as promising therapeutic targets for the treatment of AKI. Overall, our study sheds light on the critical involvement of NAT10 and ac4C RNA modification in the pathogenesis of IRI-induced renal injury, offering valuable insights for the development of novel AKI treatment strategies.

Indexed as

ac4C RNA modificationAcute kidney injuryIschemia-reperfusion injuryNAT10Renal injury

Identifiers

PMID38312597
PMCPMC10835180
OpenAlexW4390974056

What OpenQuestion 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 OpenQuestion graph.