Evidence map›Paper›PMID 32038943›Full record

ArticleCardiovascular diagnosis and therapy2019

MiR-216a accelerates proliferation and fibrogenesis via targeting PTEN and SMAD7 in human cardiac fibroblasts.

Jinsong Tao, Jingyi Wang, Chunyu Li, Weiwei Wang, Hao Yu, Jinhui Liu, Xiangqing Kong, Yan Chen

Open access · diamondAbstract read
In one paragraph

Article in Cardiovascular diagnosis and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.3field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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  15. Tiaoshen Tongluo Attenuates Fibrosis by Modulating the TGF-Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  16. hsa-miR-4443 inhibits myocardial fibroblast proliferation by targeting THBS1 to regulate TGF-β1/α-SMA/collagen signaling in atrial fibrillation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
  17. Observational
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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 3 institutions in 1 country.

Jinsong TaoDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Jingyi WangDepartment of Breast Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Chunyu LiIntensive Care Unit, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Weiwei WangIntensive Care Unit, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Hao YuEmergency Center, Kizilsu Kirghiz Autonomous Prefecture People's Hospital, Artux 845350, China.
Jinhui LiuDepartment of Gynecology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Xiangqing KongDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yan ChenEmergency Center, Kizilsu Kirghiz Autonomous Prefecture People's Hospital, Artux 845350, China.
Nanjing Medical University · CNJiangsu Province Hospital · CNTibet Autonomous Region People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHeart failure (HF) is a progressive disease with relatively poor prognosis and lacks effective therapy, and the discovery of dysregulated microRNAs (miRNAs) and their role in cardiac fibroblasts have provided a new avenue for elucidating the mechanism involved in HF.

methodsTwo datasets of GSE53080 and GSE57338 were used to screen the miRNAs profiling and analysis the differentially expressed genes (DEGs) in HF. QRT-PCR was used to detect miR-216a between HF and healthy controls (HC). Cell counting kit-8 (CCK-8) assay and clonogenic assay were used to analyze the effect of proliferation and fibrogenesis. Then dual-luciferase activity assay and western blotting were used to confirm the key mechanism.

resultsIn this study, the results showed that miR-216a was significantly up-regulated in HF and over-expression of miR-216a promoted proliferation and enhanced the fibrogenesis in the human cardiac fibroblasts (HCF) cells. Phosphatase and tensin homolog (PTEN) and mothers against decapentaplegic homolog 7 (SMAD7) were both validated as the direct target genes of miR-216a, which were confirmed by the dual-luciferase reporter assay. MiR-216a decreased the expression of PTEN and SMAD7 leading to the activation of Akt/mTOR and TGF-βRI/Smad2 in the HCF cells, which might act as a promoter of cardiac fibrosis.

conclusionsOur study might provide a promising approach for the treatment of HF in the future.

Indexed as

cardiac fibroblastsHeart failure (HF)miR-216amothers against decapentaplegic homolog 7 (SMAD7)phosphatase and tensin homolog (PTEN)

Identifiers

PMID32038943
PMCPMC6987511
OpenAlexW2995290670

What OpenQuestion holds

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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.