Evidence map›Paper›PMID 30279549›Full record

ArticleScientific reports2018

Simvastatin Protects Cardiomyocytes Against Endotoxin-induced Apoptosis and Up-regulates Survivin/NF-κB/p65 Expression.

Lana Nežić, Ranko Škrbić, Ljiljana Amidžić, Radoslav Gajanin, Kamil Kuča, Vesna Jaćević

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Cardiotoxicity as a Possible Side Effect of Statins.Reviews in cardiovascular medicine · 2023
    Review
  13. Article
  14. Review of Recent Laboratory and Experimental Data on Cardiotoxicity of Statins.Journal of cardiovascular development and disease · 2022
    Review
  15. Article
  16. PeerJ · 2022
    Article
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 3 institutions in 3 countries.

Lana NežićDepartment of Pharmacology, Toxicology and Clinical Pharmacology, School of Medicine, University of Banja Luka, 14 Save Mrkalja St, 78000, Banja Luka, Bosnia and Herzegovina.
Ranko ŠkrbićDepartment of Pharmacology, Toxicology and Clinical Pharmacology, School of Medicine, University of Banja Luka, 14 Save Mrkalja St, 78000, Banja Luka, Bosnia and Herzegovina.
Ljiljana AmidžićInstitute of Pathology, University Clinical Center of Republic of Srpska, School of Medicine, University of Banja Luka, 12 Beba St, 78000, Banja Luka, Bosnia and Herzegovina.
Radoslav GajaninInstitute of Pathology, University Clinical Center of Republic of Srpska, School of Medicine, University of Banja Luka, 12 Beba St, 78000, Banja Luka, Bosnia and Herzegovina.
Kamil KučaDepartment of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanského 62, 500 03, Hradec Králové, Czech Republic. kamil.kuca@uhk.cz.ORCID http://orcid.org/0000-0001-9664-1109
Vesna JaćevićDepartment of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanského 62, 500 03, Hradec Králové, Czech Republic.
University of Banja Luka · BAMilitary Medical Academy · RSUniversity of Hradec Králové · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study is aimed to investigate whether simvastatin induces cardiomyocytes survival signaling in endotoxin (lipopolysaccharide, LSP)-induced myocardial injury, and if so, further to determine a role of survivin in simvastatin-anti-apoptotic effect. Wistar rats were pretreated with simvastatin (10-40 mg/kg po) before a single non-lethal dose of LPS. In myocardial tissue, LPS induced structural disorganization of myofibrils with significant inflammatory infiltrate (cardiac damage score, CDS = 3.87 ± 0.51, p < 0.05), whereas simvastatin dose-dependently abolished structural changes induced by LPS (p < 0.01). Simvastatin in 20 mg/kg and 40 mg/kg pretreatment, dose dependently, attenuated myocardial apoptosis determined as apoptotic index (28.8 ± 4.5% and 18.9 ± 3.5, p < 0.05), decreased cleaved caspase-3 expression (32.1 ± 5.8%, p < 0.01), along with significant Bcl-xL expression in the simvastatin groups (p < 0.01). Interestingly, in the simvastatin groups were determined significantly increased expression of survivin (p < 0.01), but in negative correlation with cleaved caspase-3 and apoptotic indices (p < 0.01). Simvastatin has a cardioprotective effects against LPS induced apoptosis. The effect may be mediated by up-regulation of survivin via activation of NF-κB, which leads to reduced activation of caspase-3 and consequent apoptosis of cardiomyocytes in experimental sepsis.

Indexed as

Administration, OralAnimalsApoptosisCardiomyopathiesCaspase 3Cell SurvivalDisease Models, AnimalDose-Response Relationship, DrugEscherichia coliHeartHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLipopolysaccharidesMaleMyocardiumMyocytes, CardiacBirc5 protein, ratCasp3 protein, ratCaspase 3Hydroxymethylglutaryl-CoA Reductase InhibitorsLipopolysaccharidesRela protein, ratSimvastatinSurvivinTranscription Factor RelA

Identifiers

PMID30279549
PMCPMC6168467
OpenAlexW2893883302

What OpenQuestion holds

Textmetadata
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.