Evidence map›Paper›PMID 36240130›Full record

ArticlePloS one2022

Endothelial derived miRNA-9 mediated cardiac fibrosis in diabetes and its regulation by ZFAS1.

Biao Feng, Jieting Liu, Eric Wang, Zhaoliang Su, Subrata Chakrabarti

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Review
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  7. Article
  8. Mechanistic insight into the role of cardiac-enriched microRNAs in diabetic heart injury.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  9. Article
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  11. Article
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  14. Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023
    Review
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  17. 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

5 authors at 2 institutions in 2 countries.

Biao FengDepartment of Pathology and Laboratory Medicine, Western University, London, Ontario, Canada.ORCID 0000-0001-7523-5478
Jieting LiuDepartment of Pathology and Laboratory Medicine, Western University, London, Ontario, Canada.
Eric WangDepartment of Pathology and Laboratory Medicine, Western University, London, Ontario, Canada.ORCID 0000-0001-5140-5567
Zhaoliang SuJiangsu University, Zhenjiang, China.
Subrata ChakrabartiDepartment of Pathology and Laboratory Medicine, Western University, London, Ontario, Canada.
Western University · CAJiangsu University · CN

Funding

CIHR 173414
6 · The paper itself

Abstract

Diabetic cardiomyopathy (DCM) is one of the most prevalent causes of morbidity and mortality in diabetic patients. Hyperglycemia induces increased expression/deposition of extracellular matrix (ECM) proteins including fibronectin (FN) and collagen (Col) and plays an important role in fibrosis in diabetic cardiomyopathy (DCM). The roles of RNAs including microRNA (miRNA) and long non-coding RNAs (lncRNA) have begun to be understood in many conditions. In this study, we investigated the role of a specific miRNA, miR-9, and its interactions with lncRNA ZFAS1 in mediating fibrosis in DCM. Treatment with 25 mM glucose (HG) decreased miR-9 expression and increased expressions of ZFAS1, ECM proteins and inflammatory markers, compared to 5 mM glucose (NG) in the HCMECs by using qRT-PCR. Glucose-induced upregulation of ECM proteins can be prevented by ZFAS1 siRNA or miR-9 mimic transfection. Luciferase assay was confirmed miR-9 binding to FN 3'-UTR. miR-9 expression can be regulated by ZFAS1 through polycomb repressive complex 2 (PRC2) components using RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays. In the in vivo experiment, hyperglycemia-induced the ECM production can be prevented by the miR-9 overexpression in the fibrosis in DCM. These studies showed a novel glucose-induced molecular mechanism in which ZFAS1 participates in the transcriptional regulation of ECM protein production in diabetes through miR-9.

Indexed as

Diabetes MellitusDiabetic CardiomyopathiesHyperglycemiaMicroRNAsRNA, Long NoncodingExtracellular Matrix ProteinsFibronectinsFibrosisGlucoseHumansPolycomb Repressive Complex 2RNA, Small InterferingExtracellular Matrix ProteinsFibronectinsGlucoseMicroRNAsPolycomb Repressive Complex 2RNA, Long NoncodingRNA, Small InterferingZFAS1 long non-coding RNA, human

Identifiers

PMID36240130
PMCPMC9565427
OpenAlexW4306181067

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.