Evidence map›Paper›PMID 41408178›Full record

ArticleBMC nephrology2025

MicroRNA-107 alleviates ferroptosis-mediated acute kidney injury by regulating the PI3K/Akt/mTOR pathway.

Pengfei Zhao, Zhenghua Wu, Hua Chen

Abstract read
In one paragraph

Article in BMC nephrology, 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

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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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

3 authors.

Pengfei ZhaoOrgan transplant center, Tongji Shanxi Hospital, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Taiyuan, 030032, China.
Zhenghua WuOrgan transplant center, Tongji Shanxi Hospital, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Taiyuan, 030032, China.
Hua ChenOrgan transplant center, Tongji Shanxi Hospital, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Taiyuan, 030032, China. yzzxchenhua11@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMechanistic pathways and biomarkers need to be explored to elucidate the pathogenesis of acute kidney injury (AKI). This study examined miR-107 expression in AKI and the molecular mechanisms underlying the regulation of ferroptosis-mediated AKI.

methodsThis study included 30 patients with AKI and 30 healthy individuals in the control group. The miR-107 serum expression levels were determined using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The HK-2 cells were subjected to ferroptosis in vitro, and a AKI mice model to study the effect of miR-107 in vivo. After RNA overexpression, malondialdehyde (MDA), lipid reactive oxygen species (ROS), and glutathione (GSH) levels were measured. Additionally, the regulatory relationship between miR-107 and its downstream pathway genes was analyzed.

resultsThe down-regulated expression of miR-107 detected in the serum of patients with AKI suggested its utility as a potential diagnostic indicator for AKI. Moreover, miR-107 expression was down-regulated in both HK-2 cell models of AKI and HK-2 cell ferroptosis model. Upregulation of miR-107 decreased MDA expression and increased GSH expression in erastin (Era)-induced ferroptosis in HK-2 cells in vitro. Additional, AKI mice exhibited down-regulated expression levels of miR-107, and the ROS, MDA, and GSH expression changes in AKI mice were rescued after miR-107 overexpressed, which was consistent with the effect of Fer-1 treatment. Furthermore, the PI3K/Akt/mTOR pathway exhibited a correlation with miR-107 expression in Era-induced ferroptosis in HK-2 cells.

conclusionIn summary, miR-107 is expressed at low levels in AKI and can inhibit ferroptosis in HK-2 cells, which may play a protective role against AKI.

Indexed as

Acute Kidney InjuryFerroptosisMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAnimalsCell LineDown-RegulationFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedSignal TransductionMicroRNAsMIRN107 microRNA, humanMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAcute kidney injuryFerroptosismiR-107PI3K/Akt/mTOR

Identifiers

PMID41408178
PMCPMC12821974

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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.