Evidence map›Paper›PMID 33033152›Full record

ArticleThe European respiratory journal2020

Cellular senescence: friend or foe to respiratory viral infections?

William J Kelley, Rachel L Zemans, Daniel R Goldstein

Open access · bronzeAbstract read
In one paragraph

Article in The European respiratory journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  6. [Mechanism and significance of cell senescence induced by viral infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
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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

3 authors at 1 institution in 1 country.

William J KelleyDept of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Rachel L ZemansDept of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Daniel R GoldsteinDept of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0001-6695-979X
University of Michigan · US

Funding

Training Program in Molecular HematologyT32HL007622 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SUNG WON CHOI, Jordan A. Shavit · 1986 to 2026
$9.2M
Mechanisms to augment primary immunity in agingR01AG028082 · NIA · YALE UNIVERSITY · PI DENG, JANE C · 2007 to 2023
$6.9M
Physician Scientist Training in Age-Related DiseasesT32AG062403 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MIN, LILLIAN CHIANG, MODY, LONA · 2020 to 2025
$2.7M
Mechanisms of Repair of the Alveolar Epithelium after Lung InjuryR01HL131608 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ZEMANS, RACHEL LYNNE · 2016 to 2020
$1.9M
Aging and Innate Immune Mechanisms in Pulmonary InfectionR01HL130669 · NHLBI · YALE UNIVERSITY · PI BUCALA, RICHARD J, GOLDSTEIN, DANIEL ROBERT · 2015 to 2018
$1.7M
Novel Inflammatory Pathway of Aged-Enhanced AtherosclerosisR01HL127687 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GOLDSTEIN, DANIEL ROBERT · 2016 to 2019
$1.6M
Role of TGFβ/BMP Antagonism in Regeneration of the Alveolar Epithelium After Lung InjuryR01HL147920 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ZEMANS, RACHEL LYNNE · 2020 to 2021
$992k
Academic leadership in the Biology of Aging and Cardiovascular DiseasesK07AG050096 · NIA · YALE UNIVERSITY · PI GOLDSTEIN, DANIEL ROBERT · 2015 to 2019
$651k
NHLBI NIH HHS R01 HL127687NHLBI NIH HHS R01 HL130669NHLBI NIH HHS R01 HL131608NHLBI NIH HHS R01 HL147920NHLBI NIH HHS T32 HL007622NIA NIH HHS K07 AG050096NIA NIH HHS R01 AG028082NIA NIH HHS T32 AG062403
6 · The paper itself

Abstract

Cellular senescence permanently arrests the replication of various cell types and contributes to age-associated diseases. In particular, cellular senescence may enhance chronic lung diseases including COPD and idiopathic pulmonary fibrosis. However, the role cellular senescence plays in the pathophysiology of acute inflammatory diseases, especially viral infections, is less well understood. There is evidence that cellular senescence prevents viral replication by increasing antiviral cytokines, but other evidence shows that senescence may enhance viral replication by downregulating antiviral signalling. Furthermore, cellular senescence leads to the secretion of inflammatory mediators, which may either promote host defence or exacerbate immune pathology during viral infections. In this Perspective article, we summarise how senescence contributes to physiology and disease, the role of senescence in chronic lung diseases, and how senescence impacts acute respiratory viral infections. Finally, we develop a potential framework for how senescence may contribute, both positively and negatively, to the pathophysiology of viral respiratory infections, including severe acute respiratory syndrome due to the coronavirus SARS-CoV-2.

Indexed as

Cellular SenescenceHumansLungRespiratory Tract InfectionsVirus Diseases

Identifiers

PMID33033152
PMCPMC7758538
OpenAlexW3092153370

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.