Evidence map›Paper›PMID 40485171›Full record

ArticleRenal failure2025

Direct scavenging of ROS by S-PPE NP reduces oxidative stress-induced stimulation of the SESN2/AMPK/KIM-1 pathway in acute kidney injury.

Chen Jiao, Hengyi Li, Yongdong Wu, Lemei Hu, Fengzhang Huang, Ming Liang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Renal failure, 2025. 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. Review
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

6 authors.

Chen JiaoDepartment of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, PR China.
Hengyi LiDepartment of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, PR China.
Yongdong WuDepartment of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, PR China.
Lemei HuDepartment of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, PR China.
Fengzhang HuangDepartment of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, PR China.
Ming LiangDepartment of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious research demonstrated that treatment of acute kidney injury (AKI) with the antioxidant S-PPE NP reduced the levels of the oxidative stress-responsive protein Sestrin2 (SESN2), and suggested that kidney injury molecule 1 (KIM-1) could serve as a biomarker for early tubular injury. A comprehensive elucidation of the regulatory effects of S-PPE NP on SESN2 and KIM-1 expression in ischemia-reperfusion injury-AKI (IRI-AKI) could enhance therapeutic approaches for AKI. MATERIALS AND

methodsAn

resultsSignificant upregulation of SESN2 and KIM-1 was observed in both H/R and IRI models, which was attenuated following S-PPE NP treatment. Overexpression of SESN2 resulted in enhanced AMPK phosphorylation and reduced KIM-1 levels, whereas inhibition of AMPK phosphorylation with compound C did not affect SESN2 levels but led to an increase in KIM-1 levels.

conclusionSESN2 serves as a protective factor in the initial phase of renal IRI-AKI, facilitating renal repair by promoting AMPK phosphorylation, which subsequently suppresses KIM-1 expression. Moreover, S-PPE NPs effectively mitigate IRI-AKI by directly scavenging reactive oxygen species and reducing SESN2 expression.

Indexed as

Acute Kidney InjuryAntioxidantsHepatitis A Virus Cellular Receptor 1Reactive Oxygen SpeciesReperfusion InjurySestrinsAMP-Activated Protein KinasesAnimalsCell LineDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLOxidative StressPhosphorylationAMP-Activated Protein KinasesAntioxidantsHAVCR1 protein, humanHavcr1 protein, mouseHepatitis A Virus Cellular Receptor 1Reactive Oxygen SpeciesSESN2 protein, humanSesn2 protein, mouseSestrinsAcute kidney injuryischemia–reperfusion injuryoxidative stresssens2

Identifiers

PMID40485171
PMCPMC12150639

What Socratic holds

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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.