Evidence map›Paper›PMID 28624189›Full record

ArticleMolecular therapy. Nucleic acids2017

Mir30c Is Involved in Diabetic Cardiomyopathy through Regulation of Cardiac Autophagy via BECN1.

Chen Chen, Shenglan Yang, Huaping Li, Zhongwei Yin, Jiahui Fan, Yanru Zhao, Wei Gong, Mengwen Yan, Dao Wen Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.1field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. MicroRNAs in cardiovascular diseases.Medical review (2021) · 2022
    Review
  18. Article
  19. Article
  20. 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 3 institutions in 1 country.

Chen ChenDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China.
Shenglan YangDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China; Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400046, China.
Huaping LiDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China.
Zhongwei YinDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China.
Jiahui FanDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China.
Yanru ZhaoDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China.
Wei GongDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China.
Mengwen YanDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China.
Dao Wen WangDivision of Cardiology, Department of Internal Medicine, Institute of Hypertension, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (Huazhong University of Science and Technology), Wuhan 430030, China. Electronic address: dwwang@tjh.tjmu.edu.cn.
Tongji Hospital · CNHuazhong University of Science and Technology · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple factors have been shown to promote the progression of diabetic cardiomyopathy. A link has previously been found between Mir30 and autophagy in cancer cells and in the heart, but the role of Mir30 in diabetic heart has not been studied. Using in vitro and in vivo approaches, we found that the depletion of Mir30c and induction of BECN1 enhanced autophagy in diabetic (db/db) hearts and in cardiomyocytes treated with the fatty acid palmitate. We verified that Mir30c repressed BECN1 expression by direct binding to the BECN1 3' UTRs. Mir30c overexpression inhibited the induction of BECN1 and subsequent autophagy in diabetic hearts and improved cardiac function and structure in diabetic mice. However, these effects were abrogated by BECN1 overexpression. Similarly, Mir30c knockdown resulted in increased BECN1 levels and autophagic flux, aggravating cardiac abnormalities. We also show that SP1, an important transcriptional factor in energy metabolism regulation, is a key upstream activator of Mir30c that binds the promoter region of Mir30c. Our findings indicate that downregulation of Mir30c and subsequent activation of BECN1 promotes autophagy, contributing to the pathogenesis of diabetic cardiomyopathy. This observation suggests a theoretical ground for developing microRNA-based therapeutics against diabetic cardiomyopathy by inhibiting autophagy.

Indexed as

autophagyBECN1cardiac dysfunctiondiabetesMir30c

Identifiers

PMID28624189
PMCPMC5415963
OpenAlexW2601616556

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.