Evidence map›Paper›PMID 30443172›Full record

ArticleInternational journal of medical sciences2018

Simvastatin Protects Heart from Pressure Overload Injury by Inhibiting Excessive Autophagy.

Feifei Su, Miaoqian Shi, Jian Zhang, Qiangsun Zheng, Dongwei Zhang, Wei Zhang, Haichang Wang, Xue Li

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-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

9 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  7. Implications on the Therapeutic Potential of StatinsOxidative medicine and cellular longevity · 2021
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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

8 authors at 1 institution in 1 country.

Feifei SuDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Miaoqian ShiDepartment of Cardiology, PLA Army General Hospital, No.5 Nanmen Cang, Dongcheng District, Beijing, 100700, China.
Jian ZhangDepartment of Cardiology, Beijing Chest Hospital Heart Center, Capital Medical University, No.9. Beiguan Grand Street, Tongzhou District, Beijing, 101149, China.
Qiangsun ZhengDivision of Cardiology, Second Affiliated Hospital of JiaoTong University, Xi'an, 710004, China.
Dongwei ZhangDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Wei ZhangDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Haichang WangDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Xue LiDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy is an independent predictor of cardiovascular morbidity and mortality. To identify the mechanisms by which simvastatin inhibits cardiac hypertrophy induced by pressure overload, we determined effects of simvastatin on 14-3-3 protein expression and autophagic activity. Simvastatin was administered intragastrically to Sprague-Dawley (SD) rats before abdominal aortic banding (AAB). Neonatal rat cardiomyocytes (NRCs) were treated with simvastatin before angiotensin II (AngII) stimulation. 14-3-3, LC3, and p62 protein levels were determined by western blot. Autophagy was also measured by the double-labeled red fluorescent protein-green fluorescent protein autophagy reporter system. Simvastatin alleviated excessive autophagy, characterized by a high LC3II/LC3I ratio and low level of p62, and blunted cardiac hypertrophy while increasing 14-3-3 protein expression in rats that had undergone AAB. In addition, it increased 14-3-3 expression and inhibited excessive autophagy in NRCs exposed to AngII. Our study demonstrated that simvastatin may inhibit excessive autophagy, increase 14-3-3 expression, and finally exert beneficial effects on cardioprotection against pressure overload.

Indexed as

14-3-3 ProteinsAnimalsAutophagyBlotting, WesternCells, CulturedHypertrophyMaleMicroscopy, ConfocalMyocytes, CardiacRatsRats, Sprague-DawleySimvastatin14-3-3 ProteinsSimvastatin14-3-3autophagyhydroxymethylglutaryl-CoA reductase inhibitorshypertrophysimvastatin

Identifiers

PMID30443172
PMCPMC6216062
OpenAlexW2898396517

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.