Evidence map›Paper›PMID 32351959›Full record

ArticleFrontiers in cell and developmental biology2020

LncRNA-MIAT-Mediated miR-214-3p Silencing Is Responsible for IL-17 Production and Cardiac Fibrosis in Diabetic Cardiomyopathy.

Yanqing Qi, Hongyu Wu, Changjiang Mai, Hanqun Lin, Jia Shen, Xiaoyun Zhang, Yakun Gao, Yong Mao, Xupin Xie

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.6field-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

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

  1. Pooled it
  2. LncRNA SNHG14 drives alveolar inflammation in bronchopulmonary dysplasia via DNMT3a-mediated epigenetic silencing of miR-214-3p.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. The heart of diabetes: unraveling metabolic drivers of cardiomyopathy.Cardiovascular diabetology. Endocrinology reports · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. The immunology of diabetic cardiomyopathy.Frontiers in endocrinology · 2025
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024
    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 2 institutions in 1 country.

Yanqing QiDepartment of Cardiovascular Surgery, Ningbo First Hospital, Ningbo, China.
Hongyu WuDepartment of Cardiovascular Surgery, Ningbo First Hospital, Ningbo, China.
Changjiang MaiDepartment of Cardiovascular Surgery, Ningbo First Hospital, Ningbo, China.
Hanqun LinDepartment of Cardiovascular Surgery, Ningbo First Hospital, Ningbo, China.
Jia ShenDepartment of Cardiovascular Surgery, Ningbo First Hospital, Ningbo, China.
Xiaoyun ZhangDepartment of Cardiovascular Surgery, Ningbo First Hospital, Ningbo, China.
Yakun GaoDepartment of Cardiovascular Surgery, Ningbo First Hospital, Ningbo, China.
Yong MaoDepartment of Cardiovascular Surgery, Ningbo First Hospital, Ningbo, China.
Xupin XieDepartment of Vascular Surgery, School of Medicine, Affiliated Hangzhou First People's Hospital, Zhejiang University, Hangzhou, China.
Ningbo First Hospital · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As an important complication of diabetes mellitus, diabetic cardiomyopathy (DCM) is characterized by a silent development in its earlier stage and a deficient cardiomyocyte contractility in its late stage. So far, little advance has been achieved to reverse this pathological change. LncRNAs are defined as a large cluster of RNAs without the function of encoding proteins, but have the capacity in controlling gene expression. Interleukin-17 (IL-17), a proinflammatory cytokine, is a key regulator of host inflammation. Clinically, it plays a crucial role in the pathogenesis of cardiac interstitial fibrosis. In this study, we reported that high glucose-induced lncRNA-MIAT upregulation is responsible for proinflammatory IL-17 production in cardiomyocytes. The underlying mechanism is likely due to that lncRNA-MIAT specific attenuates miR-214-3p-mediated inhibitory effect on IL-17 expression. As a result, attenuated IL-17 expression significantly ameliorate cardiac fibrosis, followed by improvement of cardiac contractility. Taken together, our study first suggests that lncRNA-MIAT plays a key role in DCM and targeting lncRNA-MIAT may become a potential strategy to treat DCM.

Indexed as

diabetic cardiomyopathyfibrosisIL-17lncRNA-MIATmiR-214-3p

Identifiers

PMID32351959
PMCPMC7174588
OpenAlexW3016459825

What OpenQuestion 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 OpenQuestion graph.