Evidence map›Paper›PMID 41811913›Full record

ArticleJournal of immunology research2026

MicroRNA-382 Is Involved in Acute Kidney Injury via Regulating STAT1 Signaling.

Xiaoyan Wang, Guo Cheng, Ting Ren, Zhouping Zou, Xinni Zhang, Shuan Zhao, Siyu Bao, Yingxiang Li, Ping Jia, Yi Fang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of immunology research, 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

11 authors.

Xiaoyan WangDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.ORCID https://orcid.org/0000-0001-7047-0110
Guo ChengInternational Medical Center, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.
Ting RenDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.
Zhouping ZouClinical Research Unit, Institute of Clinical Science, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.ORCID https://orcid.org/0000-0001-5835-3405
Xinni ZhangDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.
Shuan ZhaoDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.
Siyu BaoDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.
Yingxiang LiDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.
Ping JiaDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.ORCID https://orcid.org/0000-0002-0608-161X
Yi FangDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.ORCID https://orcid.org/0000-0001-8675-4513
Xiaoqiang DingDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China, zs-hospital.sh.cn.ORCID https://orcid.org/0000-0002-5269-2868

Funding

National Natural Science Foundation of China 82170695National Natural Science Foundation of China 91849123Science and Technology Commission of Shanghai Municipality 14DZ2260200Science and Technology Commission of Shanghai Municipality 20DZ2271600
6 · The paper itself

Abstract

Acute kidney injury (AKI), characterized by inflammation and oxidative stress, is a life-threatening clinical presentation. We previously demonstrated the role of miR-382 in the progression of chronic kidney disease (CKD). However, the role of miR-382 in AKI is unknown. Genetic depletion of miR-382 exacerbated renal dysfunction, histologic lesions, apoptosis of epithelial cells, and oxidative stress in kidneys in ischemia-reperfusion (I/R)- and sepsis-induced AKI. In vitro, downregulation of miR-382 accompanied with activation of phosphorylation of signal transducer and activator of transcription 1 (STAT1) were induced in mouse renal tubular epithelial cells (mTECs) with hypoxia/reoxygenation (H/R) and lipopolysaccharide (LPS) treatments. Colocalization of phosphorylated STAT1 (p-STAT1) and Lotus tetragonolobus lectin (LTL) suggested the activation of STAT1 signaling in renal epithelial after I/R injury (IRI). Overexpression of miR-382 in mTECs abrogated phosphorylation of STAT1, generation of interleukin-6 (Il-6), tumor necrosis factor-α (Tnf-α), and Il-1β as well as reactive oxygen species (ROS) and apoptosis after H/R- and LPS treatments. Additionally, loss of miR-382 was found in isolated macrophages from kidney during I/R-induced AKI. Upregulation of miR-382 in Raw264.7 cells inactivated STAT1 signaling and hindered polarization of M1 macrophages inhibiting Il-6 and inducible nitric oxide synthase (iNos). Inhibition of STAT1 pharmacologically reduced Il-1β, Il-6, and Tnf-α in Raw264.7 after H/R. Taken together, these results demonstrated the protective role of miR-382 in I/R- and sepsis-induced AKI, suggesting miR-382 as a novel therapeutic strategy for AKI.

Indexed as

Acute Kidney InjuryMicroRNAsSTAT1 Transcription FactorAnimalsApoptosisCytokinesDisease Models, AnimalEpithelial CellsHumansLipopolysaccharidesMacrophagesMaleMiceOxidative StressPhosphorylationReactive Oxygen SpeciesCytokinesLipopolysaccharidesMicroRNAsReactive Oxygen SpeciesStat1 protein, mouseSTAT1 Transcription Factoracute kidney injurymacrophagesmicroRNAtubular epithelial cells

Identifiers

PMID41811913
PMCPMC13140935

What OpenQuestion 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 OpenQuestion graph.