Evidence map›Paper›PMID 34390301›Full record

ArticleIUBMB life2022

Endoplasmic reticulum stress and NF-kB activation in SARS-CoV-2 infected cells and their response to antiviral therapy.

Desirée Bartolini, Anna Maria Stabile, Carmine Vacca, Alessandra Pistilli, Mario Rende, Antimo Gioiello, Gabriele Cruciani, Francesco Galli

Open access · hybridAbstract read
In one paragraph

Article in IUBMB life, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  18. SARS-CoV-2PeerJ · 2023
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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.

Desirée BartoliniDepartment of Chemistry, Biology and Biotechnology, University of Perugia, Perugia, Italy.ORCID 0000-0003-3849-757X
Anna Maria StabileDepartment of Medicine and Surgery, Section of Human, Clinical and Forensic Anatomy, University of Perugia, Perugia, Italy.ORCID 0000-0003-1047-4210
Carmine VaccaDepartment of Chemistry, Biology and Biotechnology, University of Perugia, Perugia, Italy.ORCID 0000-0002-3799-8164
Alessandra PistilliDepartment of Medicine and Surgery, Section of Human, Clinical and Forensic Anatomy, University of Perugia, Perugia, Italy.ORCID 0000-0002-4740-2504
Mario RendeDepartment of Medicine and Surgery, Section of Human, Clinical and Forensic Anatomy, University of Perugia, Perugia, Italy.
Antimo GioielloApplied Biochemistry and Nutrition Lab, Department of Pharmaceutical Sciences, University of Perugia, Perugia, Italy.ORCID 0000-0003-0240-2006
Gabriele CrucianiDepartment of Chemistry, Biology and Biotechnology, University of Perugia, Perugia, Italy.ORCID 0000-0002-4162-8692
Francesco GalliApplied Biochemistry and Nutrition Lab, Department of Pharmaceutical Sciences, University of Perugia, Perugia, Italy.ORCID 0000-0003-3626-051X
University of Perugia · IT

Funding

Fondazione Cassa di Risparmio di Perugia 19,837 (2020.0522)
6 · The paper itself

Abstract

Unfolded protein response (UPR) and endoplasmic reticulum (ER) stress are aspects of SARS-CoV-2-host cell interaction with proposed role in the cytopathic and inflammatory pathogenesis of this viral infection. The role of the NF-kB pathway in these cellular processes remains poorly characterized. When investigated in VERO-E6 cells, SARS-CoV-2 infection was found to markedly stimulate NF-kB protein expression and activity. NF-kB activation occurs early in the infection process (6 hpi) and it is associated with increased MAPK signaling and expression of the UPR inducer IRE-1α. These signal transduction processes characterize the cellular stress response to the virus promoting a pro-inflammatory environment and caspase activation in the host cell. Inhibition of viral replication by the viral protease inhibitor Nelfinavir reverts all these molecular changes also stimulating c-Jun expression, a key component of the JNK/AP-1 pathway with important role in the IRE-1α-mediated transcriptional regulation of stress response genes with anti-inflammatory and cytoprotection function. The present study demonstrates that UPR signaling and its interaction with cellular MAPKs and the NF-kB activity are important aspects of SARS-CoV-2-host cell interaction that deserve further investigation to identify more efficient therapies for this viral infection.

Indexed as

COVID-19 Drug TreatmentSARS-CoV-2Adenosine MonophosphateAlanineAnimalsAntiviral AgentsCaspase 9Chlorocebus aethiopsCOVID-19Cytopathogenic Effect, ViralEndoplasmic Reticulum StressHumansMAP Kinase Signaling SystemModels, BiologicalNelfinavirNF-kappa BAdenosine MonophosphateAlanineAntiviral AgentsCaspase 9NelfinavirNF-kappa Bremdesivirc-JunCOVID-19inflammationNelfinavirNF-kBRemdesivirSARS-CoV-2stress responseVERO-E6 cells

Identifiers

PMID34390301
PMCPMC8426894
OpenAlexW3192766782

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.