Evidence map›Paper›PMID 33014208›Full record

ReviewInflammation and regeneration2020

How COVID-19 induces cytokine storm with high mortality.

Shintaro Hojyo, Mona Uchida, Kumiko Tanaka, Rie Hasebe, Yuki Tanaka, Masaaki Murakami, Toshio Hirano

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Inflammation and regeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05212532 (A Proof-of-Concept Study Evaluating Safety, Tolerability, and Preliminary Efficacy of EOM613 in COVID-19 Infected Patients With Severe Symptoms), which is not on this map. Cited by 408 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
408citing papers in PubMed, 9 pooled it
14.9field-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.

NCT05212532 phase1unknown statusnot on this mapstarted 2021, after this paper: background citation

A Proof-of-Concept Study Evaluating Safety, Tolerability, and Preliminary Efficacy of EOM613 in COVID-19 Infected Patients With Severe Symptoms

TypeinterventionalSponsorEOM PharmaceuticalsRan2021 to 2022Enrolled40ConditionsCOVID-19 Pneumonia, COVID-19 Respiratory Infection, COVID-19 Acute Respiratory Distress SyndromeArmsEOM613
3 · Its place in the literature

Who cites it

408 citing papers in PubMed, 9 syntheses or guidelines pooled it, 693 citations in OpenAlex.

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  8. Antidepressants for COVID-19: A systematic review.Journal of affective disorders · 2022
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348 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

7 authors at 1 institution in 1 country.

Shintaro Hojyo *Molecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Hokkaido, 060-0815 Japan.
Mona Uchida *Molecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Hokkaido, 060-0815 Japan.
Kumiko TanakaMolecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Hokkaido, 060-0815 Japan.
Rie HasebeMolecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Hokkaido, 060-0815 Japan.
Yuki TanakaMolecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Hokkaido, 060-0815 Japan.
Masaaki MurakamiMolecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Hokkaido, 060-0815 Japan.ORCID 0000-0001-7159-7279
Toshio HiranoMolecular Psychoimmunology, Institute for Genetic Medicine, Graduate School of Medicine, Hokkaido University, Hokkaido, 060-0815 Japan.
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The newly emerging coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in Wuhan, China, but has rapidly spread all over the world. Some COVID-19 patients encounter a severe symptom of acute respiratory distress syndrome (ARDS) with high mortality. This high severity is dependent on a cytokine storm, most likely induced by the interleukin-6 (IL-6) amplifier, which is hyper-activation machinery that regulates the nuclear factor kappa B (NF-κB) pathway and stimulated by the simultaneous activation of IL-6-signal transducer and activator of transcription 3 (STAT3) and NF-κB signaling in non-immune cells including alveolar epithelial cells and endothelial cells. We hypothesize that IL-6-STAT3 signaling is a promising therapeutic target for the cytokine storm in COVID-19, because IL-6 is a major STAT3 stimulator, particularly during inflammation. We herein review the pathogenic mechanism and potential therapeutic targets of ARDS in COVID-19 patients.

Identifiers

PMID33014208
PMCPMC7527296
OpenAlexW3091085673

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.