Evidence map›Paper›PMID 34582362›Full record

ArticleAging2021

miR-320 accelerates chronic heart failure with cardiac fibrosis through activation of the IL6/STAT3 axis.

Fang Li, Shan-Shan Li, Hui Chen, Jian-Zhi Zhao, Jie Hao, Jin-Ming Liu, Xiu-Guang Zu, Wei Cui

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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
1.3field-weighted citation impact, top 20% 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, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Exosomal miR-320c: A Novel Biomarker for Atrial Cardiomyopathy.Journal of cardiovascular translational research · 2025
    Article
  4. Article
  5. Current issues in molecular biology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Fang LiThird Division, Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, PR China.
Shan-Shan LiThird Division, Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, PR China.
Hui ChenThird Division, Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, PR China.
Jian-Zhi ZhaoDepartment of Biochemistry and Molecular Biology, The Hebei Medical University, Shijiazhuang, Hebei 050011, PR China.
Jie HaoThird Division, Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, PR China.
Jin-Ming LiuThird Division, Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, PR China.
Xiu-Guang ZuThird Division, Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, PR China.
Wei CuiDepartment of Cardiology, The Second Hospital of Hebei Medical University and Hebei Institute of Cardiovascular Research, Shijiazhuang, Hebei 050011, PR China.
Second Hospital of Hebei Medical University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibrosis could induce abnormal cardiac function and become a novel target for cardiac hypertrophy and chronic heart failure. MiRNA-320 is a crucial miRNA in cardiovascular disease, but it is poorly understood whether it plays a role in cardiac fibrosis pathogenesis. We aimed to identify the specific underlying mechanism of miR-320 in cardiac fibrosis and hypertrophic pathogenesis. In our study, the GEO datasets revealed that STAT3 was significantly highly expressed in cardiomyocyte lines. MiR-320 activation and STAT3 signaling pathways were statistically significantly connected. Furthermore, miR-320 was highly associated with cardiac fibrosis and hypertrophic disease. Interstitial fibrosis was observed in the mice subjected to TAC surgery, markedly enhanced in miR-320 mimics. Mechanistically, we revealed that miR-320 mimics aggravated the pressure overload and induced cardiac hypertrophy and fibrosis via the IL6/STAT3/PTEN axis. MiR-320 mimics accelerated cardiac hypertrophy and cardiac fibrosis via the IL6/STAT3/PTEN axis. These results suggest that targeting miR-320 may represent a potential therapeutic strategy for cardiac hypertrophy and fibrosis.

Indexed as

AnimalsCardiomegalyCells, CulturedDatasets as TopicDisease Models, AnimalFibrosisHeart FailureInterleukin-6MiceMicroRNAsMyocytes, CardiacSTAT3 Transcription FactorInterleukin-6MicroRNAsMirn320 microRNA, mouseSTAT3 protein, humanSTAT3 Transcription Factorcardiac fibrosischronic heart failureIL6/STAT3/PTEN axismiR-320

Identifiers

PMID34582362
PMCPMC8507257
OpenAlexW3203057140

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.