Evidence map›Paper›PMID 33691172›Full record

ReviewMicrobial pathogenesis2021

Contribution of STAT3 to the pathogenesis of COVID-19.

Abdollah Jafarzadeh, Maryam Nemati, Sara Jafarzadeh

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Microbial pathogenesis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05062681 (Randomized Controlled Trial on the Efficacy of Dexamethasone Versus Methyl Prednisolone in Covid-19 Infected Patients With High Oxygen Flow), which is not on this map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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.

NCT05062681 phase4unknown statusnot on this map

Randomized Controlled Trial on the Efficacy of Dexamethasone Versus Methyl Prednisolone in Covid-19 Infected Patients With High Oxygen Flow

TypeinterventionalSponsorCairo UniversityRan2021 to 2022Enrolled60ConditionsCOVID-19 PandemicArmsDexamethasone, Methylprednisolone
3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Observational
  11. Article
  12. Classification and regulatory interactions of key transcription factors in COVID-19.Frontiers in cellular and infection microbiology · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
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  20. Article

5 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

3 authors at 1 institution in 1 country.

Abdollah JafarzadehDepartment of Immunology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran; Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Electronic address: Jafarzadeh14@yahoo.com.
Maryam NematiImmunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran; Department of Hematology and Laboratory Sciences, School of Para-Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Sara JafarzadehStudent Research Committee, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Kerman University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyper-inflammatory responses, lymphopenia, unbalanced immune responses, cytokine storm, large viral replication and massive cell death play fundamental roles in the pathogenesis of COVID-19. Extreme production of many kinds of pro-inflammatory cytokines and chemokines occur in severe COVID-19 that called cytokine storm. Signal transducer and activator of transcription-3 (STAT-3) present in the cytoplasm in an inactive form and can be stimulated by a vast range of cytokines, chemokines and growth factors. Thus, STAT-3 can participate in the induction of inflammatory responses during coronavirus infections. STAT-3 can also suppress anti-virus interferon response and induce unbalanced anti-virus adaptive immune response, through influencing Th17-, Th1-, Treg-, and B cell-mediated functions. Furthermore, STAT-3 can contribute to the M2 macrophage polarization, lung fibrosis and thrombosis. Moreover, STAT-3 may be directly targeted by some virus-derived protein and operate as a pro-viral or anti-viral element in a virus-specific process. Here, the possible contribution of STAT-3 to the pathogenesis of COVID-19 was explained, while providing potential approaches to target this transcription factor in an attempt for COVID-19 treatment.

Indexed as

Coronavirus InfectionsCOVID-19 Drug TreatmentCytokine Release SyndromeCytokinesHumansSARS-CoV-2STAT3 Transcription FactorCytokinesSTAT3 protein, humanSTAT3 Transcription FactorCOVID-19Immune responseInflammationPathogenesisSARS-CoV-2STAT3Treatment

Identifiers

PMID33691172
PMCPMC7937040
OpenAlexW3134123677

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.