Evidence map›Paper›PMID 41201583›Full record

ArticleArchives of toxicology2026

Depleted uranium exposure induced ferroptosis in renal cells via the ETHE1/P38-MAPK pathway.

Feng Huang, Wenrun Li, Juan Li, Yonghong Ran, Shiyan Fu, Li Shen, Qi Li, Xiaoyu Yang, Yazhen Zhao, Yuhui Hao

Abstract read
PubMed Publisher
In one paragraph

Article in Archives of toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

10 authors.

Feng Huang *State Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Wenrun Li *State Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Juan LiState Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Yonghong RanState Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Shiyan FuState Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Li ShenState Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Qi LiState Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Xiaoyu YangState Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Yazhen ZhaoState Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.
Yuhui HaoState Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China. yuhuihao@tmmu.edu.cn.ORCID 0000-0002-7161-2624

Funding

Science and Technology Research Program of Chongqing Municipal Education Commission KJQN202412806
6 · The paper itself

Abstract

This study investigated the role of ferroptosis in acute depleted uranium (DU)-induced nephrotoxicity. Using Sprague-Dawley rats and HK-2 cells to establish models of acute DU exposure (rats: 10 mg/kg; cells: 500 μM for 24 h), we found that DU exposure caused mitochondrial dysfunction, lipid peroxidation, and iron accumulation, all hallmarks of ferroptosis, which were inhibited by ferrostatin-1 (Fer-1). We identified mitochondrial ethylmalonic encephalopathy 1 (ETHE1) as a key DU target. ETHE1 downregulation exacerbated DU-induced reactive oxygen species (ROS), ferrous ions (Fe

Indexed as

FerroptosisMitochondrial Proteinsp38 Mitogen-Activated Protein KinasesAnimalsCell LineHumansKidneyMaleMAP Kinase Signaling SystemRatsRats, Sprague-DawleyReactive Oxygen SpeciesMitochondrial Proteinsp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesDepleted uraniumETHE1FerritinophagyFerroptosisP38-MAPK

Identifiers

PMID41201583

What Socratic holds

Textmetadata
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.