Evidence map›Paper›PMID 32257391›Full record

ArticleCell death discovery2020

LncRNA GAS5 promotes apoptosis as a competing endogenous RNA for miR-21 via thrombospondin 1 in ischemic AKI.

Xuemei Geng, Nana Song, Shuan Zhao, Jiarui Xu, Yong Liu, Yi Fang, Mingyu Liang, Xialian Xu, Xiaoqiang Ding

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

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  10. Epigenetic Regulation by lncRNA GAS5/miRNA/mRNA Network in Human Diseases.International journal of molecular sciences · 2025
    Review
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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

9 authors at 4 institutions in 2 countries.

Xuemei Geng1Department of Nephrology, Zhongshan Hospital, Fudan University; Shanghai Institute of Kidney and Dialysis; Shanghai Key Laboratory of Kidney and Blood Purification; Shanghai Medical Center of Kidney Disease, Shanghai, China.
Nana Song1Department of Nephrology, Zhongshan Hospital, Fudan University; Shanghai Institute of Kidney and Dialysis; Shanghai Key Laboratory of Kidney and Blood Purification; Shanghai Medical Center of Kidney Disease, Shanghai, China.
Shuan Zhao1Department of Nephrology, Zhongshan Hospital, Fudan University; Shanghai Institute of Kidney and Dialysis; Shanghai Key Laboratory of Kidney and Blood Purification; Shanghai Medical Center of Kidney Disease, Shanghai, China.
Jiarui Xu1Department of Nephrology, Zhongshan Hospital, Fudan University; Shanghai Institute of Kidney and Dialysis; Shanghai Key Laboratory of Kidney and Blood Purification; Shanghai Medical Center of Kidney Disease, Shanghai, China.
Yong Liu2Department of Physiology and Center of Systems Molecular Medicine, Medical College of Wisconsin, Milwaukee, WI USA.
Yi Fang1Department of Nephrology, Zhongshan Hospital, Fudan University; Shanghai Institute of Kidney and Dialysis; Shanghai Key Laboratory of Kidney and Blood Purification; Shanghai Medical Center of Kidney Disease, Shanghai, China.
Mingyu Liang2Department of Physiology and Center of Systems Molecular Medicine, Medical College of Wisconsin, Milwaukee, WI USA.
Xialian Xu1Department of Nephrology, Zhongshan Hospital, Fudan University; Shanghai Institute of Kidney and Dialysis; Shanghai Key Laboratory of Kidney and Blood Purification; Shanghai Medical Center of Kidney Disease, Shanghai, China.
Xiaoqiang Ding1Department of Nephrology, Zhongshan Hospital, Fudan University; Shanghai Institute of Kidney and Dialysis; Shanghai Key Laboratory of Kidney and Blood Purification; Shanghai Medical Center of Kidney Disease, Shanghai, China.
Zhongshan Hospital · CNMedical College of Wisconsin · USShanghai Institute of Hematology · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence has indicated that long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) played important roles in renal ischemia/reperfusion (I/R) injury. However, the involvement of lncRNA growth arrest specific 5 (GAS5) in acute kidney injury (AKI) remained largely unexplored. This study aimed to determine possible mechanisms of GAS5 in the renal I/R process. We found that GAS5, noticeably upregulated by renal I/R injury, was further suppressed by delayed IPC while knockdown of miR-21 in vivo before IPC could significantly increased the GAS5 levels. Concurrently, TSP-1 was negatively regulated by miR-21 in vivo and vitro. Additionally, Reciprocal repression of GAS5 and miR-21 was identified. Knockdown of miR-21 in H6R0.5 treated HK-2 cells promoted apoptosis. Co-transfection of miR-21 mimic and pcDNA-GAS5 or pcDNA-Vector were performed, results of which showed that inhibition of miR-21 on TSP-1 could be rescued by overexpression of GAS5. This study suggested that GAS5 facilitated apoptosis by competitively sponging miR-21, which negatively regulated TSP-1 in renal I/R injury. This novel regulatory axis could act as a therapeutic target for AKI in the future.

Indexed as

Acute kidney injuryGene regulationLong non-coding RNAs

Identifiers

PMID32257391
PMCPMC7118150
OpenAlexW3014920575

What OpenQuestion holds

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LicenceCC BY
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.