Evidence map›Paper›PMID 32384619›Full record

ReviewInternational journal of molecular sciences2020

Cellular Senescence in the Lung: The Central Role of Senescent Epithelial Cells.

Christine Hansel, Verena Jendrossek, Diana Klein

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
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  12. IFN-Mediated Bronchial Epithelium Cellular Senescence in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. The vascular endothelium as decision maker in lung injury.Frontiers in cell and developmental biology · 2025
    Review

1 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

3 authors at 1 institution in 1 country.

Christine HanselInstitute of Cell Biology (Cancer Research), University of Duisburg-Essen, University Hospital Essen, Virchowstrasse 173, 45122 Essen, Germany.
Verena JendrossekInstitute of Cell Biology (Cancer Research), University of Duisburg-Essen, University Hospital Essen, Virchowstrasse 173, 45122 Essen, Germany.ORCID 0000-0003-1058-2107
Diana KleinInstitute of Cell Biology (Cancer Research), University of Duisburg-Essen, University Hospital Essen, Virchowstrasse 173, 45122 Essen, Germany.ORCID 0000-0002-1770-443X
Essen University Hospital · DE

Funding

Bundesministerium für Bildung und Forschung 02NUK047DDeutsche Forschungsgemeinschaft GRK1739/2
6 · The paper itself

Abstract

Cellular senescence is a key process in physiological dysfunction developing upon aging or following diverse stressors including ionizing radiation. It describes the state of a permanent cell cycle arrest, in which proliferating cells become resistant to growth-stimulating factors. Senescent cells differ from quiescent cells, which can re-enter the cell cycle and from finally differentiated cells: morphological and metabolic changes, restructuring of chromatin, changes in gene expressions and the appropriation of an inflammation-promoting phenotype, called the senescence-associated secretory phenotype (SASP), characterize cellular senescence. The biological role of senescence is complex, since both protective and harmful effects have been described for senescent cells. While initially described as a mechanism to avoid malignant transformation of damaged cells, senescence can even contribute to many age-related diseases, including cancer, tissue degeneration, and inflammatory diseases, particularly when senescent cells persist in damaged tissues. Due to overwhelming evidence about the important contribution of cellular senescence to the pathogenesis of different lung diseases, specific targeting of senescent cells or of pathology-promoting SASP factors has been suggested as a potential therapeutic approach. In this review, we summarize recent advances regarding the role of cellular (fibroblastic, endothelial, and epithelial) senescence in lung pathologies, with a focus on radiation-induced senescence. Among the different cells here, a central role of epithelial senescence is suggested.

Indexed as

Cellular SenescenceAlveolar Epithelial CellsAnimalsDNA ReplicationHumansStress, Physiologicalcancer therapyionizing radiationlung injurypulmonary diseaseradiotherapySASPsenescence-associated secretory phenotype

Identifiers

PMID32384619
PMCPMC7247355
OpenAlexW3022891041

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.