Evidence map›Paper›PMID 26149640›Full record

ArticleJournal of nephrology2016

Elevation of miR-21, through targeting MKK3, may be involved in ischemia pretreatment protection from ischemia-reperfusion induced kidney injury.

Zhihui Li, Xu Deng, Zhijuan Kang, Ying Wang, Tuanhong Xia, Niu Ding, Yan Yin

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 24% of its field
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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

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  19. The Yin-Yang Regulation of Reactive Oxygen Species and MicroRNAs in Cancer.International journal of molecular sciences · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Zhihui LiDepartment of Nephrology of Hunan Children's Hospital, Hunan Institute for Pediatric Research, 86 Ziyuan Road, Changsha, 410007, Hunan, People's Republic of China. lizhihuimedsci@126.com.
Xu DengDepartment of Nephrology of Hunan Children's Hospital, Hunan Institute for Pediatric Research, 86 Ziyuan Road, Changsha, 410007, Hunan, People's Republic of China.
Zhijuan KangDepartment of Nephrology of Hunan Children's Hospital, Hunan Institute for Pediatric Research, 86 Ziyuan Road, Changsha, 410007, Hunan, People's Republic of China.
Ying WangDepartment of Nephrology of Hunan Children's Hospital, Hunan Institute for Pediatric Research, 86 Ziyuan Road, Changsha, 410007, Hunan, People's Republic of China.
Tuanhong XiaDepartment of Nephrology of Hunan Children's Hospital, Hunan Institute for Pediatric Research, 86 Ziyuan Road, Changsha, 410007, Hunan, People's Republic of China.
Niu DingDepartment of Nephrology of Hunan Children's Hospital, Hunan Institute for Pediatric Research, 86 Ziyuan Road, Changsha, 410007, Hunan, People's Republic of China.
Yan YinDepartment of Nephrology of Hunan Children's Hospital, Hunan Institute for Pediatric Research, 86 Ziyuan Road, Changsha, 410007, Hunan, People's Republic of China.
Hunan Children's Hospital · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIschemia-reperfusion (IR) causes acute kidney injury (AKI), and ischemia pretreatment may exert protection. Mitogen-activated protein kinase kinase 3 (MKK3), which is involved in the signal transduction pathway in IR-induced injury, is a potential target of miR-21. We aimed to verify the targeting regulation of miR-21 on MKK3 and to explore the effects of miR-21-mediated MKK3 expression changes in AKI.

methodsVectors containing the MKK3 3'UTR and mutated MKK3-3U-M were constructed and co-transfected with nonsense miR, miR-21-5p mimics or inhibitor in HEK293 cells. Gene expressions were detected by dual luciferase reporter assay. The effects of miR-21 on mRNA and protein of MKK3 were investigated in HK-2 cells. Male C57BL/6J mice were treated with ischemic preconditioning (IPC) and IR. Kidney functions were assessed through monitoring serum creatinine (Scr) and blood urea nitrogen (BUN). Pathological changes were observed and scored with histological samples of kidney. Expression levels of miR-21, MKK3, interleukin (IL)-6, tumor necrosis factor (TNF)-α before and after IPC and IR were examined by real-time polymerase chain reaction and/or immunohistochemistry.

resultsmiR-21 regulated the expression of MKK3 via 3'UTR. Following IR, MKK3, IL-6 and TNF-α levels were increased. Scr, BUN and pathological injuries were aggravated, and miR-21 expression was increased. IPC increased miR-21 levels ahead of IR and inhibited the increases in MKK3, IL-6 and TNF-α levels and the aggravation of Scr, BUN and pathological injuries.

conclusionsmiR-21 targets MKK3 in vivo and in vitro, inhibiting the downstream factors IL-6 and TNF-α. Therefore, miR-21 might be involved in protection of IPC against IR of the kidney.

Indexed as

Ischemic Preconditioning3' Untranslated RegionsAcute Kidney InjuryAnimalsBinding SitesBiomarkersBlood Urea NitrogenCreatinineDisease Models, AnimalHEK293 CellsHumansInterleukin-6KidneyMaleMAP Kinase Kinase 3Mice, Inbred C57BL3' Untranslated RegionsBiomarkersCreatinineInterleukin-6interleukin-6, mouseMAP2K3 protein, humanMap2k3 protein, mouseMAP Kinase Kinase 3MicroRNAsMIRN21 microRNA, humanMIRN21 microRNA, mouseTumor Necrosis Factor-alphaAcute kidney injuryIschemia preconditioningMitogen-activated protein kinase 3p38 mitogen-activated protein kinase

Identifiers

PMID26149640
OpenAlexW914766842

What OpenQuestion 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 OpenQuestion graph.