Evidence map›Paper›PMID 35034538›Full record

ArticleBioengineered2022

miR-129-5p restores cardiac function in rats with chronic heart failure by targeting the E3 ubiquitin ligase Smurf1 and promoting PTEN expression.

Yuan Qi, Yan Tang, Lu Yin, Keke Ding, Cuimei Zhao, Wenwen Yan, Yi'an Yao

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024
    Review
  8. Article
  9. Article
  10. Noncoding RNAs and Cardiac Fibrosis.Reviews in cardiovascular medicine · 2023
    Review
  11. Article
  12. Review
  13. Article
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 4 institutions in 1 country.

Yuan QiDepartment of Cardiology, Gongli Hospital of Shanghai Pudong New Area, Shanghai, China.
Yan TangDepartment of Cardiology, Tongji Hospital Affiliated to Tongji University, Shanghai, China.
Lu YinDepartment of Cardiology, Gongli Hospital of Shanghai Pudong New Area, Shanghai, China.
Keke DingDepartment of Cardiology, Tongji Hospital Affiliated to Tongji University, Shanghai, China.
Cuimei ZhaoDepartment of Cardiology, Tongji Hospital Affiliated to Tongji University, Shanghai, China.
Wenwen YanDepartment of Cardiology, Tongji Hospital Affiliated to Tongji University, Shanghai, China.
Yi'an YaoDepartment of Cardiology, Tongji Hospital Affiliated to Tongji University, Shanghai, China.
Tongji University · CNTongji Hospital · CNSecond Military Medical University · CNShanghai Pudong New Area Gongli Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic heart failure (CHF) is a prevalent health concern with complex pathogenesis. This current study set out to estimate the function of the miR-129-5p/Smurf1/PTEN axis on cardiac function injury in CHF. The model of CHF in rats was established. The cardiac function indexes, myocardial tissue damage, and oxidative stress-related factors in CHF rats were evaluated after the interference of Smurf1/miR-129-5p/PTEN. The targeting relationships between miR-129-5p and Smurf1 and between PTEN and Smurf1 were verified. It was found that that after modeling, cardiac functions were impaired, heart/left ventricular/lung weight and the myocardial structure was destroyed, and the degree of fibrosis of myocardial tissue was increased. After Smurf1 knockdown, the cardiac function, myocardial structure, and oxidative stress were improved, and the fibrosis in myocardial tissue was decreased. Smurf1 was a target of miR-129-5p. miR-129-5p could annul the protective effect of Smurf1 silencing on CHF rats. Smurf1 inhibited PTEN expression by promoting PTEN ubiquitination, while miR-129-5p enhanced PTEN expression by inhibiting Smurf1. Meanwhile, overexpression of PTEN annulled the cardiac dysfunction in CHF rats induced by Smurf1. In conclusion, miR-129-5p targeted Smurf1 and repressed the ubiquitination of PTEN, and promoted PTEN expression, thus improving the cardiac function of CHF rats.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsChronic DiseaseHeart FailureMaleMicroRNAsPTEN PhosphohydrolaseRatsRats, WistarUbiquitin-Protein LigasesMicroRNAsMIRN129 microRNA, ratPTEN PhosphohydrolasePten protein, ratSmurf1 protein, ratUbiquitin-Protein Ligasescardiac dysfunctionChronic heart failureE3 ubiquitin ligase Smurf1miR-129-5pPTENubiquitination

Identifiers

PMID35034538
PMCPMC8974089
OpenAlexW4206560490

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.