Evidence map›Paper›PMID 31631065›Full record

ArticleAging2019

Long noncoding RNA GAS5 inhibits cell proliferation and fibrosis in diabetic nephropathy by sponging miR-221 and modulating SIRT1 expression.

Xiaoxu Ge, Bojin Xu, Wenwei Xu, Lili Xia, Zhongqin Xu, Lisha Shen, Wenfang Peng, Shan Huang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
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  7. Epigenetic Regulation by lncRNA GAS5/miRNA/mRNA Network in Human Diseases.International journal of molecular sciences · 2025
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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

8 authors at 1 institution in 1 country.

Xiaoxu GeDepartment of Endocrinology, Tongren Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
Bojin XuDepartment of Endocrinology, Tongren Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
Wenwei XuDepartment of Geriatrics, Tongren Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
Lili XiaDepartment of Endocrinology, Tongren Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
Zhongqin XuDepartment of Family Medicine, Tongren Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
Lisha ShenDepartment of Endocrinology, Tongren Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
Wenfang PengDepartment of Endocrinology, Tongren Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
Shan HuangDepartment of Endocrinology, Tongren Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China.
Tongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is one of the leading causes of end-stage renal diseases worldwide. This study is designed to investigate the underlying function and mechanism of a novel lncRNA GAS5 in the progression of DN. We found that lncRNA GAS5 expression level was decreased in type 2 diabetes (T2D) with DN compared with that in patients without DN. Moreover, lncRNA GAS5 expression level was negatively associated with the severity of DN-related complications. lncRNA GAS5 inhibited MCs proliferation and caused G0/1 phase arrest. lncRNA GAS5 overexpression alleviated the expression of fibrosis-related protein in mesangial cells (MCs). The dual-luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay results revealed that lncRNA GAS5 functions as an endogenous sponge for miR-221 via both the directly targeting way and Ago2-dependent manner. Furthermore, SIRT1 was confirmed as a target gene of miR-221. lncRNA GAS5 upregulated SIRT1 expression and inhibited MCs proliferation and fibrosis by acting as an miR-221 sponge. Finally, we found that lncRNA GSA5 suppressed the development of DN in vivo. Thus, lncRNA GAS5 was involved in the progression of DN by sponging miR-221 and contributed to lncRNA-directed diagnostics and therapeutics in DN.

Indexed as

AgingAnimalsArgonaute ProteinsCell ProliferationDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisGene DeletionGene Expression RegulationGlucoseMaleMesangial CellsMiceMicroRNAsRatsRats, Sprague-DawleyAgo2 protein, mouseAgo2 protein, ratArgonaute ProteinsGlucoselong non-coding RNA GAS5, mouseMicroRNAsMIRN221 microRNA, mouseRNA, Long NoncodingSirt1 protein, mouseSirtuin 1diabetic nephropathyfibrosislncRNA GAS5proliferation

Identifiers

PMID31631065
PMCPMC6834398
OpenAlexW2981743892

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.