Evidence map›Paper›PMID 32636055›Full record

ReviewCytokine & growth factor reviews2020

The potential of JAK/STAT pathway inhibition by ruxolitinib in the treatment of COVID-19.

Bakiye Goker Bagca, Cigir Biray Avci

Open access · greenAbstract readReview
In one paragraph

Review in Cytokine & growth factor reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 2 pooled it
11.5field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 2 syntheses or guidelines pooled it, 120 citations in OpenAlex.

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  16. Adverse drug reactions associated with COVID-19 management.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  17. Review
  18. Article
  19. Mechanisms ofOpen medicine (Warsaw, Poland) · 2024
    Article
  20. Exogenous Klotho Extends Survival in COVID-19 Model Mice.Pathogens (Basel, Switzerland) · 2023
    Article

11 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

2 authors at 1 institution in 1 country.

Bakiye Goker BagcaDepartment of Medical Biology, Medical Faculty, Ege University, Izmir, Turkey. Electronic address: bakiye.goker.bagca@ege.edu.tr.
Cigir Biray AvciDepartment of Medical Biology, Medical Faculty, Ege University, Izmir, Turkey.
Ege University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ruxolitinib is the first approved JAK1 and JAK2 inhibitor, and is known to interfere with the JAK / STAT signaling pathway, one of the critical cellular signaling pathways involved in the inflammatory response. This review presents an overview of SARS-CoV-2 and the COVID-19 pandemic, and then focuses on the potential efficacy of ruxolitinib in this infection. The potential targets of ruxolitinib were determined by using genetic alterations that have been reported in COVID-19 patients. The potential effectiveness of ruxolitinib is suggested by evaluating the interactions of these potential targets with ruxolitinib or JAK/STAT pathway.

Indexed as

Antiviral AgentsBetacoronavirusCoronavirus InfectionsCOVID-19Cytokine Release SyndromeHumansJanus Kinase 1Janus Kinase 2Janus Kinase InhibitorsNitrilesPandemicsPneumonia, ViralPyrazolesPyrimidinesRisk FactorsSARS-CoV-2Antiviral AgentsJAK1 protein, humanJAK2 protein, humanJanus Kinase 1Janus Kinase 2Janus Kinase InhibitorsNitrilesPyrazolesPyrimidinesruxolitinibSTAT Transcription FactorsCOVID-19Cytokine stormJAK/STAT pathwayRuxolitinibSARS-CoV-2

Identifiers

PMID32636055
PMCPMC7305753
OpenAlexW3035765027

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.