Evidence map›Paper›PMID 32968640›Full record

ArticleCardiovascular diagnosis and therapy2020

MiR-181c protects cardiomyocyte injury by preventing cell apoptosis through PI3K/Akt signaling pathway.

Xiaoli Li, Jiuchang Zhong, Zhen Zeng, Hongjiang Wang, Jing Li, Xiaoyan Liu, Xinchun Yang

Open access · diamondAbstract read
In one paragraph

Article in Cardiovascular diagnosis and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026
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  10. Investigating the Mechanism of Action ofDrug design, development and therapy · 2023
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  13. Cardioprotective Mechanism and Active Compounds ofComputational and mathematical methods in medicine · 2022
    Article
  14. Recent Advances in Gene Therapy for Cardiac Tissue Regeneration.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Non-coding RNAs in Cardiac Regeneration.Frontiers in physiology · 2021
    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

7 authors at 3 institutions in 1 country.

Xiaoli LiDepartment of Cardiology, Chaoyang Hospital affiliated to Capital Medical University, Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, China.
Jiuchang ZhongDepartment of Cardiology, Chaoyang Hospital affiliated to Capital Medical University, Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, China.
Zhen ZengGeriatric Department, Chui Yang Liu Hospital Affiliated to Tsinghua University, Beijing, China.
Hongjiang WangDepartment of Cardiology, Chaoyang Hospital affiliated to Capital Medical University, Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, China.
Jing LiDepartment of Cardiology, Chaoyang Hospital affiliated to Capital Medical University, Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, China.
Xiaoyan LiuDepartment of Cardiology, Chaoyang Hospital affiliated to Capital Medical University, Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, China.
Xinchun YangDepartment of Cardiology, Chaoyang Hospital affiliated to Capital Medical University, Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, China.
Beijing Chao-Yang Hospital · CNCapital Medical University · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiomyocyte apoptosis plays an important role in the development of heart failure, which leads to high mortality in patients with cardiovascular diseases. In this study, we are focused to identify the role of miRNA-181c in the regulating of myocardial tissue apoptosis in the doxorubicin (DOX) or hypoxia/reoxygenation (H/R) induced H9C2 cardiomyocyte injury.

methodsDOX-induced heart failure animal model was established using mice. Total RNA was extracted from tissue and cell using Trizol. RT-PCR was conducted for real-time RNA quantification. H9c2 cells were collected and labeled using an Annexin V-PI apoptosis kit. Flow cytometry was conducted to identify the cell apoptosis. Rat cardiomyocyte H9c2 cell was treated by 16 hours' hypoxia and 2 hours' reoxygenation to induce cell apoptosis. TUNEL assay was employed for myocardial tissue apoptosis analysis.

resultsIt was revealed that miR-181c was suppressed on the heart tissue of DOX-induced heart failure animal model. We observed miR-181c overexpression reduced apoptosis through TUNEL assay, which suggested the inhibitory effect of miR-181c on myocardial tissue apoptosis. Transfection of miR-181c mimic could decrease cell apoptosis in H/R treated H9C2 cells

conclusionsOur study revealed that miR-181c protected heart failure by impeding cardiomyocyte apoptosis through PI3K/Akt pathway, implying the therapeutic role of miR-181c during the exacerbation of the cardiovascular disease.

Indexed as

cardiomyocyte apoptosisdoxorubicinhypoxia/reoxygenation (H/R)miR-181cPI3K/Akt

Identifiers

PMID32968640
PMCPMC7487411
OpenAlexW3048245233

What OpenQuestion holds

Textmetadata
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.