Evidence map›Paper›PMID 33875647›Full record

ArticleCell death discovery2021

Overexpression of circRNA SNRK targets miR-103-3p to reduce apoptosis and promote cardiac repair through GSK3β/β-catenin pathway in rats with myocardial infarction.

Yeqian Zhu, Pengcheng Zhao, Ling Sun, Yao Lu, Wenwu Zhu, Jian Zhang, Chengyu Xiang, Yangming Mao, Qiushi Chen, Fengxiang Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
  3. Review
  4. Review
  5. Empagliflozin modulates microRNA expression in human primary cardiomyocytes under CoClInternational journal of cardiology. Cardiovascular risk and prevention · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. CircRNA-mediated regulation of cardiovascular disease.Frontiers in cardiovascular medicine · 2024
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. The Landscape of Circular RNAs in Cardiovascular Diseases.International journal of molecular sciences · 2023
    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

10 authors at 2 institutions in 1 country.

Yeqian Zhu *Section of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Pengcheng Zhao *Section of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Ling SunSection of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Yao LuSection of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Wenwu ZhuSection of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Jian ZhangSection of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Chengyu XiangSection of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Yangming MaoSection of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Qiushi ChenSection of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Fengxiang ZhangSection of Pacing and Electrophysiology, Division of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China. njzfx6@njmu.edu.cn.ORCID http://orcid.org/0000-0003-0125-3926
Nanjing Medical University · CNChangzhou No.2 People's Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81871113National Natural Science Foundation of China (National Science Foundation of China) 81901410
6 · The paper itself

Abstract

Ischemic cardiomyopathy seriously endangers human health leading to a poor prognosis. Acute myocardial infarction (AMI) is the primary etiology, and the pathophysiological process concludes with the death of cardiomyocytes caused by acute and persistent ischemia and hypoxia in the coronary arteries. We identified a circRNA (circSNRK) which was downregulated in rats with myocardial infarction (MI), however, the role it plays in the MI environment is still unclear. This study contained experiments to investigate the role of circSNRK in the regulation of cardiac survival and explore the mechanisms underlying circSNRK functions. Quantitative real-time PCR (qRT-PCR) was performed to determine the circSNRK expression patterns in hearts. Gain-of-function assays were also conducted in vitro and in vivo to determine the role of circSNRK in cardiac repair. qRT-PCR, western blot, and luciferase reporter assays were used to study circRNA interactions with micro RNAs (miRNAs). Overexpression of circSNRK in cardiomyocytes reduced apoptosis and increased proliferation. Adeno associated virus 9 (AAV9) mediated myocardium overexpression of circSNRK in post MI hearts reduced cardiomyocyte apoptosis, promoted cardiomyocyte proliferation, enhanced angiogenesis, and improved cardiac functions. Overall, upregulation of circSNRK promotes cardiac survival and functional recovery after MI. Mechanistically, circSNRK regulates cardiomyocyte apoptosis and proliferation by acting as a miR-103-3p sponge and inducing increased expression of SNRK which can bind GSK3β to regulate its phosphorylated activity. And thus circSNRK may be a promising therapeutic target for improving clinical prognosis after MI.

Identifiers

PMID33875647
PMCPMC8055694
OpenAlexW3153844368

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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.