Evidence map›Paper›PMID 34311128›Full record

ArticleBiomedical journal2022

LncRNA OIP5-AS1 reduces renal epithelial cell apoptosis in cisplatin-induced AKI by regulating the miR-144-5p/PKM2 axis.

Siyuan Chang, Mingyang Chang, Gang Liu, Daqian Xu, Haili Wang, Rongqing Sun, Min Feng

Open access · goldAbstract read
In one paragraph

Article in Biomedical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Siyuan ChangDepartment of SICU, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province, PR China.
Mingyang ChangDepartment of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province, PR China.
Gang LiuDepartment of SICU, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province, PR China.
Daqian XuDepartment of SICU, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province, PR China.
Haili WangDepartment of SICU, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province, PR China.
Rongqing SunDepartment of SICU, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province, PR China.
Min FengDepartment of SICU, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan Province, PR China. Electronic address: minfenguniversity@163.com.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe abnormal expression of long non-coding RNA (lncRNA) Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) has been observed in many human cancers and the underlying mechanisms have been well studied. However, the function of OIP5-AS1 in acute kidney injury (AKI) remains unclear.

methodsTo explore the role of OIP5-AS1 in the progression of AKI, the cisplatin-induced AKI mouse and cell model were established. To confirm the potential protective effect of OIP5-AS1 during cisplatin-induced AKI, rescue experiments were performed. Targetscan was used to predict the potential targets of miR-144-5p. To further determine whether the effect of miR-144-5p during cisplatin-induced AKI was mediated by PMK2, the recuse experiments using PMK2 overexpressing vector was applied.

resultsOIP5-AS1 was significantly downregulated both in cisplatin-induced AKI mice and human renal tubular cell line HK-2 cells. Moreover, overexpression of OIP5-AS1 efficiently promoted cell growth and reduced cisplatin-induced apoptosis of HK-2 cells. Furthermore, OIP5-AS1 was identified as a sponge of miR-144-5p, and upregulation of miR-144-5p could significantly reverse overexpression of OIP5-AS1-induced protective effect on the damage of cisplatin to HK-2 cells. In addition, pyruvate kinase M2 (PKM2) was found to be a direct target of miR-144-5p, and overexpression of PKM2 efficiently reversed the effect of miR-144-5p mimics on the damage in cisplatin-stimulated HK-2 cells.

conclusionsOIP5-AS1 reduced the apoptosis of cisplatin-stimulated renal epithelial cells by targeting the miR-144-5p/PKM2 axis, which extended the regulatory network of lncRNAs in cisplatin-induced AKI and also provided a novel therapeutic target for AKI treatment.

Indexed as

Acute Kidney InjuryMicroRNAsPyruvate KinaseRNA, Long NoncodingAnimalsApoptosisCisplatinEpithelial CellsHumansMiceCisplatinMicroRNAsMIRN144 microRNA, humanPyruvate KinaseRNA, Long NoncodingAKIApoptosisCell viabilitymiR-144-5pOIP5-AS1PKM2

Identifiers

PMID34311128
PMCPMC9486127
OpenAlexW3184247368

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.