Evidence map›Paper›PMID 30356256›Full record

ArticlePloS one2018

AT1-receptor blockade: Protective effects of irbesartan in cardiomyocytes under hypoxic stress.

Mariarosaria Boccellino, Marina Di Domenico, Maria Donniacuo, Giuseppe Bitti, Giulia Gritti, Pasqualina Ambrosio, Lucio Quagliuolo, Barbara Rinaldi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

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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 2 countries.

Mariarosaria BoccellinoDepartment of Precision Medicine, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Marina Di DomenicoDepartment of Precision Medicine, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.ORCID 0000-0002-6201-4200
Maria DonniacuoDepartment of Experimental Medicine, Section of Pharmacology, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Giuseppe BittiDepartment of Precision Medicine, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Giulia GrittiDepartment of Experimental Medicine, Section of Pharmacology, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Pasqualina AmbrosioDepartment of Precision Medicine, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Lucio QuagliuoloDepartment of Precision Medicine, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
Barbara RinaldiDepartment of Experimental Medicine, Section of Pharmacology, Università degli Studi della Campania "Luigi Vanvitelli", Naples, Italy.
University of Campania "Luigi Vanvitelli" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia induces myocardial injury through the activation of inflammatory and oxidative processes. The pivotal role of the renin angiotensin system (RAS) in the pathogenesis of cardiovascular diseases has been firmly established in clinical trials and practice; in fact many experimental and clinical data have highlighted that its inhibition has a cardioprotective role. Activated RAS also stimulates inflammation directly inducing proinflammatory and oxidative gene expression. This study aimed to investigate the protective role of a pre-treatment (10 and 100 μM) with irbesartan on injury induced by 24 h of hypoxia in HL-1 cardiomyocytes; in particular, we have analyzed the natriuretic peptide (BNP) expression, a biomarker able to modulate inflammatory reaction to cardiac injury and some markers involved in oxidative stress and inflammation. Our results demonstrated that a pre-treatment with 100 μM irbesartan significantly increased SOD activity and catalase expression of 15 and 25%, respectively, compared to hypoxic cells (P<0.05). On the other hand, it was able to reduce the release of peroxynitrite and iNOS protein expression of 20 and 50% respectively (P<0.05). In addition irbesartan exerts an anti-inflammatory activity reducing Toll-like receptors (TLRs)-2 and -4 mRNA expression, TNF-alpha expression and activity (20%) and increasing the expression of the cytokine IL-17 (40%) (P<0.05 vs hypoxia). Our findings also showed that BNP induced by ischemia was significantly and in a concentration-dependent manner reduced by irbesartan. The findings of our study demonstrated that the AT1 receptor antagonist irbesartan exerts a protective role in an in vitro hypoxic condition reducing oxidative stress and inflammation.

Indexed as

AnimalsCardiovascular DiseasesCatalaseGene Expression RegulationHeart InjuriesHumansHypoxiaInflammationInterleukin-17IrbesartanMiceMyocytes, CardiacOxidative StressRenin-Angiotensin SystemSuperoxide Dismutase-1Toll-Like ReceptorsCatalaseInterleukin-17IrbesartanSuperoxide Dismutase-1Toll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID30356256
PMCPMC6200178
OpenAlexW2898574977

What Socratic holds

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LicenceCC BY
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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 Socratic graph.