Evidence map›Paper›PMID 31195367›Full record

ArticleAging2019

Long non-coding RNA MEG3 promotes fibrosis and inflammatory response in diabetic nephropathy via miR-181a/Egr-1/TLR4 axis.

Fangfang Zha, Xiaolu Qu, Bo Tang, Ji Li, Yakun Wang, PengXi Zheng, Tingting Ji, Chun Zhu, Shoujun Bai

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 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.8field-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

60 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Long noncoding RNA MEG3: an active player in fibrosis.Pharmacological reports : PR · 2025
    Review
  5. Article
  6. Article
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  8. Review
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  11. Review
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  18. Review
  19. Age-related ceRNA networks in adultFrontiers in genetics · 2023
    Article
  20. Review
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 1 country.

Fangfang Zha *Department of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Qingpu District, Shanghai 201700, P.R. China.
Xiaolu Qu *Department of Nephrology, Shanghai Punan Hospital of Pudong New District, Pudong New District, Shanghai 200215, P.R. China.
Bo TangDepartment of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Qingpu District, Shanghai 201700, P.R. China.
Ji LiDepartment of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Qingpu District, Shanghai 201700, P.R. China.
Yakun WangDepartment of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Qingpu District, Shanghai 201700, P.R. China.
PengXi ZhengDepartment of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Qingpu District, Shanghai 201700, P.R. China.
Tingting JiDepartment of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Qingpu District, Shanghai 201700, P.R. China.
Chun ZhuDepartment of Nephrology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Chongming Branch, Chongming District, Shanghai 202150, P.R. China.
Shoujun BaiDepartment of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Qingpu District, Shanghai 201700, P.R. China.
Zhongshan Hospital · CNFudan University · CNPunan Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) play vital roles in diabetic nephropathy (DN). This research aimed to study the potential role and underlying molecular mechanisms of long non-coding RNA MEG3 in DN. We found that MEG3 was upregulated in DN in vivo and in vitro and could enhance cell fibrosis and inflammatory response in DN. MEG3 functioned as an endogenous sponge for miR-181a in mesangial cells (MCs) via direct targeting and in an Ago2-dependent manner. MiR-181a inhibition promoted MC fibrosis and inflammatory response. In addition, Egr-1 was confirmed as a target gene of miR-181a. Further investigations verified that MEG3 promotes fibrosis and inflammatory response via the miR-181a/Egr-1/TLR4 axis in vitro and in vivo. These results provide new insights into the regulation between MEG3 and the miR-181a/Egr-1/TLR4 signaling pathway during DN progression.

Indexed as

AnimalsCell LineCell ProliferationDiabetes Mellitus, ExperimentalDiabetic NephropathiesEarly Growth Response Protein 1FibrosisInflammationMaleMesangial CellsMiceMicroRNAsRatsRats, Sprague-DawleyRNA, Long NoncodingSignal TransductionEarly Growth Response Protein 1Egr1 protein, mouseMEG3 non-coding RNA, mouseMicroRNAsMIRN-181 microRNA, humanmirn181 microRNA, mouseRNA, Long NoncodingTlr4 protein, mouseToll-Like Receptor 4ceRNAdiabetic nephropathylncRNA MEG3miR-181a

Identifiers

PMID31195367
PMCPMC6594792
OpenAlexW2952239070

What Socratic holds

Textmetadata
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 Socratic graph.