Evidence map›Paper›PMID 38095608›Full record

ArticleAging2023

Uncovering a unique pathogenic mechanism of SARS-CoV-2 omicron variant: selective induction of cellular senescence.

Franziska Hornung, Nilay Köse-Vogel, Claude Jourdan Le Saux, Antje Häder, Lea Herrmann, Luise Schulz, Lukáš Radosa, Thurid Lauf, Tim Sandhaus, Patrick Samson and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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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

15 authors at 5 institutions in 2 countries.

Franziska HornungInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Nilay Köse-VogelInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Claude Jourdan Le SauxMedicine/Pulmonary and Critical Care Division, University of California San Francisco, San Francisco, CA 94110, USA.
Antje HäderInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Lea HerrmannInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Luise SchulzInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Lukáš RadosaInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Thurid LaufInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Tim SandhausKlinik für Herz- und Thoraxchirurgie, Jena 07747, Germany.
Patrick SamsonKlinik für Herz- und Thoraxchirurgie, Jena 07747, Germany.
Torsten DoenstKlinik für Herz- und Thoraxchirurgie, Jena 07747, Germany.
Daniel WittschieberInstitute of Forensic Medicine, Jena University Hospital, Jena 07747, Germany.
Gita MallInstitute of Forensic Medicine, Jena University Hospital, Jena 07747, Germany.
Bettina LöfflerInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Stefanie Deinhardt-EmmerInstitute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany.
Jena University Hospital · DELeibniz Institute of Photonic Technology · DEKlinik für Herzchirurgie Karlsruhe · DEUniversity of Bonn · DEUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSARS-CoV-2 variants are constantly emerging with a variety of changes in the conformation of the spike protein, resulting in alterations of virus entry mechanisms. Solely omicron variants use the endosomal clathrin-mediated entry. Here, we investigate the influence of defined altered spike formations to study their impact on premature cellular senescence.

methodsIn our study,

resultsSolely omicron variants of SARS-CoV-2 influenced the expression of cell cycle genes, highlighted by an increased p21 expression in human primary lung cells and human

conclusionsSignificant changes due to different SARS-CoV-2 infections in human primary alveolar epithelial cells with an overall impact on premature aging could be identified. A substantially different cellular response with an upregulation of cell cycle, inflammation- and integrin-associated pathways in omicron infected cells indicates premature cellular senescence.

Indexed as

COVID-19SARS-CoV-2Alveolar Epithelial CellsCellular SenescenceHumanscellular senescencelung airway cellsSARS-CoV-2variant of concern

Identifiers

PMID38095608
PMCPMC10756098
OpenAlexW4389606751

What Socratic 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 Socratic graph.