Evidence map›Paper›PMID 33072409›Full record

ReviewCell death discovery2020

The role of death domain proteins in host response upon SARS-CoV-2 infection: modulation of programmed cell death and translational applications.

Nikita V Ivanisenko, Kamil Seyrek, Nikolay A Kolchanov, Vladimir A Ivanisenko, Inna N Lavrik

Open access · goldAbstract readReview
In one paragraph

Review in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.2field-weighted citation impact, top 12% 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

41 citing papers in PubMed, 53 citations in OpenAlex.

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  20. Revisiting Regulated Cell Death Responses in Viral Infections.International journal of molecular sciences · 2022
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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

5 authors at 3 institutions in 2 countries.

Nikita V IvanisenkoThe Federal Research Center Institute of Cytology and Genetics SB RAS, Novosibirsk, Russia.
Kamil SeyrekTranslational Inflammation Research, CDS, Medical Faculty, Otto von Guericke University, Magdeburg, Germany.
Nikolay A KolchanovThe Federal Research Center Institute of Cytology and Genetics SB RAS, Novosibirsk, Russia.
Vladimir A IvanisenkoThe Federal Research Center Institute of Cytology and Genetics SB RAS, Novosibirsk, Russia.
Inna N LavrikThe Federal Research Center Institute of Cytology and Genetics SB RAS, Novosibirsk, Russia.
Institute of Cytology and Genetics · RUOtto-von-Guericke University Magdeburg · DESiberian Branch of the Russian Academy of Sciences · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current pandemic of novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) poses a significant global public health threat. While urgent regulatory measures in control of the rapid spread of this virus are essential, scientists around the world have quickly engaged in this battle by studying the molecular mechanisms and searching for effective therapeutic strategies against this deadly disease. At present, the exact mechanisms of programmed cell death upon SARS-CoV-2 infection remain to be elucidated, though there is increasing evidence suggesting that cell death pathways play a key role in SARS-CoV-2 infection. There are several types of programmed cell death, including apoptosis, pyroptosis, and necroptosis. These distinct programs are largely controlled by the proteins of the death domain (DD) superfamily, which play an important role in viral pathogenesis and host antiviral response. Many viruses have acquired the capability to subvert the program of cell death and evade the host immune response, mainly by virally encoded gene products that control cell signaling networks. In this mini-review, we will focus on SARS-CoV-2, and discuss the implication of restraining the DD-mediated signaling network to potentially suppress viral replication and reduce tissue damage.

Indexed as

Cell deathInfectionInflammasome

Identifiers

PMID33072409
PMCPMC7547561
OpenAlexW3092429882

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.