Evidence map›Paper›PMID 34688149›Full record

ReviewInternational immunopharmacology2021

The triumvirate of NF-κB, inflammation and cytokine storm in COVID-19.

Ali Attiq, Lui Jin Yao, Sheryar Afzal, Mansoor Ali Khan

Open access · greenAbstract readReview
In one paragraph

Review in International immunopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 2 pooled it
4.9field-weighted citation impact, top 4% 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

77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 103 citations in OpenAlex.

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17 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Ali AttiqDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, MAHSA University, Bandar Saujana Putra, 42610 Jenjarom, Selangor, Malaysia. Electronic address: aliattiq@mahsa.edu.my.
Lui Jin YaoKuala Balah Health Clinic (Klinik Kesihatan Kuala Balah), Kuala Balah, 17600 Jeli, Kelantan, Malaysia.
Sheryar AfzalDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, MAHSA University, Bandar Saujana Putra, 42610 Jenjarom, Selangor, Malaysia.
Mansoor Ali KhanCOVID-19 Vaccination Centres, University College London Hospitals, National Health Service, N10QH London, England.
Mahsa University · MYNational Health Service · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The coronavirus disease (COVID-19) has once again reminded us of the significance of host immune response and consequential havocs of the immune dysregulation. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) inflicts severe complications to the infected host, including cough, dyspnoea, fever, septic shock, acute respiratory distress syndrome (ARDs), and multiple organ failure. These manifestations are the consequence of the dysregulated immune system, which gives rise to excessive and unattended production of pro-inflammatory mediators. Elevated circulatory cytokine and chemokine levels are accompanied by spontaneous haemorrhage, thrombocytopenia and systemic inflammation, which are the cardinal features of life-threatening cytokine storm syndrome in advanced COVID-19 diseases. Coronavirus hijacked NF-kappa B (NF-κB) is responsible for upregulating the expressions of inflammatory cytokine, chemokine, alarmins and inducible enzymes, which paves the pathway for cytokine storm. Given the scenario, the systemic approach of simultaneous inhibition of NF-κB offers an attractive therapeutic intervention. Targeted therapies with proteasome inhibitor (VL-01, bortezomib, carfilzomib and ixazomib), bruton tyrosine kinase inhibitor (acalabrutinib), nucleotide analogue (remdesivir), TNF-α monoclonal antibodies (infliximab and adalimumab), N-acetylcysteine and corticosteroids (dexamethasone), focusing the NF-κB inhibition have demonstrated effectiveness in terms of the significant decrease in morbidity and mortality in severe COVID-19 patients. Hence, this review highlights the activation, signal transduction and cross-talk of NF-κB with regard to cytokine storm in COVID-19. Moreover, the development of therapeutic strategies based on NF-κB inhibition are also discussed herein.

Indexed as

SARS-CoV-2AnimalsChromosomes, Human, XCOVID-19Cytokine Release SyndromeExophthalmosGonadal Steroid HormonesHumansNF-kappa BSignal TransductionGonadal Steroid HormonesNF-kappa BCOVID-19Cytokine stormInflammationNF-κBNovel coronavirusSARS-CoV-2Severe acute respiratory syndrome

Identifiers

PMID34688149
PMCPMC8516728
OpenAlexW3205830933

What OpenQuestion holds

Textmetadata
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.