Evidence map›Paper›PMID 40589411›Full record

ArticleActa biochimica et biophysica Sinica2025

Modulation of ferroptosis via YY1-SLC7A11 axis in hepatic ischemia-reperfusion injury pathogenesis.

Shaochuang Wang, Baofei Jiang, Jun Cao, Ting Xu, Chengming Zhou, Xiangyou Yu, Yi Wang, Yu Xie, Lindong Ji, Guangrong Zhou and 3 more

Abstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Shaochuang WangDepartment of Hepatobiliary Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an 223300, China.
Baofei JiangDepartment of General Surgery, Shanghai Tenth People's Hospital, Shanghai 200072, China.
Jun CaoState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi 830054, China.
Ting XuHematology Research Laboratory, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an 223300, China.
Chengming ZhouState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi 830054, China.
Xiangyou YuDepartment of Critical Care Medicine, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
Yi WangDepartment of Critical Care Medicine, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
Yu XieDepartment of Hepatobiliary Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an 223300, China.
Lindong JiDepartment of Gastrointestinal Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an 223300, China.
Guangrong ZhouDepartment of Gastrointestinal Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an 223300, China.
Hao WenState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi 830054, China.
Long MaDepartment of Critical Care Medicine, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
Kun WuDepartment of Gastrointestinal Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an 223300, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

YY1 is a crucial transcription factor and plays significant roles in biological processes. However, the mechanisms of YY1 action in ischemia-reperfusion injury and its regulatory role in ferroptosis have not been extensively studied. This study aims to elucidate the molecular mechanism by which NEDD4L-mediated degradation of YY1 through ubiquitination suppresses SLC7A11 transcription, leading to the promotion of cellular ferroptosis and exacerbation of hepatic ischemia-reperfusion injury (IRI), via the integration of multiple omics sequencing datasets. An IRI-I/R mouse model is established, followed by proteomic sequencing to identify proteins that are differentially expressed during IRI. The altered expression of YY1 is validated, and

Indexed as

Amino Acid Transport System y+FerroptosisLiverReperfusion InjuryYY1 Transcription FactorAnimalsHumansMaleMiceMice, Inbred C57BLNedd4 Ubiquitin Protein LigasesUbiquitinationAmino Acid Transport System y+Nedd4l protein, mouseNedd4 Ubiquitin Protein LigasesSLC7A11 protein, humanYY1 protein, humanYy1 protein, mouseYY1 Transcription Factorferroptosishepatic ischemia-reperfusion injuryNEDD4LSLC7A11ubiquitinationYY1

Identifiers

PMID40589411
PMCPMC12536466

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.