Evidence map›Paper›PMID 37969056›Full record

ArticleAging cell2023

Circulating monocytes expressing senescence-associated features are enriched in COVID-19 patients with severe disease.

Y Lin, D F Postma, L S Steeneken, L S Melo Dos Santos, J L Kirkland, J M Espindola-Netto, T Tchkonia, M Borghesan, H R Bouma, M Demaria

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  11. Cellular senescence and kidney aging.Clinical science (London, England : 1979) · 2023
    Review
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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

10 authors at 3 institutions in 2 countries.

Y LinEuropean Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), Groningen, Netherlands.
D F PostmaDepartment of Internal Medicine and Infectious Diseases, University Medical Center Groningen (UMCG), Groningen, The Netherlands.
L S SteenekenEuropean Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), Groningen, Netherlands.
L S Melo Dos SantosEuropean Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), Groningen, Netherlands.
J L KirklandClinical Pharmacy & Pharmacology, University Medical Center Groningen (UMCG), Groningen, The Netherlands.
J M Espindola-NettoDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
T TchkoniaDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
M BorghesanEuropean Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), Groningen, Netherlands.
H R BoumaDepartment of Internal Medicine and Infectious Diseases, University Medical Center Groningen (UMCG), Groningen, The Netherlands.
M DemariaEuropean Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), Groningen, Netherlands.
University of Groningen · NLUniversity Medical Center Groningen · NLMayo Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accurate biomarkers for predicting COVID-19 severity have remained an unmet need due to an incomplete understanding of virus pathogenesis and heterogeneity among patients. Cellular senescence and its pro-inflammatory phenotype are suggested to be a consequence of SARS-CoV-2 infection and potentially drive infection-dependent pathological sequelae. Senescence-associated markers in infected individuals have been identified primarily in the lower respiratory tract, while little is known about their presence in more easily accessible bio-specimens. Here, we measured the abundance of senescence-associated signatures in whole blood, plasma and peripheral blood mononuclear cells (PBMCs) of COVID-19 patients and patients without an infection. Bulk transcriptomic and targeted proteomic assays revealed that the level of senescence-associated markers, including the senescence-associated secretory phenotype (SASP), is predictive of SARS-CoV-2 infection. Single-cell RNA-sequencing data demonstrated that a senescence signature is particularly enriched in monocytes of COVID-19 patients, partially correlating with disease severity. Our findings suggest that monocytes are prematurely induced to senescence by SARS-CoV-2 infection, might contribute to exacerbating a SASP-like inflammatory response and can serve as markers and predictors for COVID-19 and its sequelae.

Indexed as

COVID-19MonocytesDisease ProgressionHumansLeukocytes, MononuclearProteomicsSARS-CoV-2ageingcellular senescenceCOVID-19monocytesSARS-CoV-2SASP

Identifiers

PMID37969056
PMCPMC10726854
OpenAlexW4388733605

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.