Evidence map›Paper›PMID 29184185›Full record

ReviewNature reviews. Gastroenterology & hepatology2018

Cellular senescence in gastrointestinal diseases: from pathogenesis to therapeutics.

Nina Frey, Sascha Venturelli, Lars Zender, Michael Bitzer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
–field-weighted citation impact
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

46 citing papers in PubMed.

  1. Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. CSPG4 Mediates Inflammatory, Cell Death, and Senescence Responses in Enteric Glia Exposed to Clostridioides difficile Toxins.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
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  5. Article
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  7. Prognostic impact of the combination of p16International journal of clinical oncology · 2024
    Article
  8. Article
  9. Review
  10. Rejuvenating aged microglia by p16Molecular neurodegeneration · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. CD8Nature reviews. Immunology · 2022
    Review
  20. Review
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

4 authors.

Nina FreyDepartment of Internal Medicine I, University of Tuebingen, Otfried-Müller-Strasse 10, 72076 Tuebingen, Germany.
Sascha VenturelliDepartment of Internal Medicine VIII, University of Tuebingen, Otfried-Müller-Strasse 10, 72076 Tuebingen, Germany.
Lars ZenderDepartment of Internal Medicine VIII, University of Tuebingen, Otfried-Müller-Strasse 10, 72076 Tuebingen, Germany.
Michael BitzerDepartment of Internal Medicine I, University of Tuebingen, Otfried-Müller-Strasse 10, 72076 Tuebingen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescence is a durable cell cycle arrest that can be induced in response to various stress factors, such as telomere erosion, DNA damage or the aberrant activation of oncogenes. In addition to its well-established role as a stress response programme, research has revealed important physiological roles of senescence in nondisease settings, such as embryonic development, wound healing, tissue repair and ageing. Senescent cells secrete various cytokines, chemokines, matrix remodelling proteases and growth factors, a phenotype collectively referred to as the senescence-associated secretory phenotype. These factors evoke immune responses that, depending on the pathophysiological context, can either prevent or even fuel disease and tumorigenesis. Remarkably, even the gut microbiota can influence senescence in various organs. In this Review, we provide an introduction to cellular senescence, addressed particularly to gastroenterologists and hepatologists, and discuss the implications of senescence for the pathogenesis of malignant and nonmalignant gastrointestinal and hepatobiliary diseases. We conclude with an outlook on how modulation of cellular senescence might be used for therapeutic purposes.

Indexed as

Biomarkers, TumorCarcinogenesisCellular SenescenceChemokinesCytokinesGastrointestinal DiseasesGastrointestinal MicrobiomeHumansImmunity, CellularLiver DiseasesPancreatic NeoplasmsBiomarkers, TumorChemokinesCytokines

Identifiers

What OpenQuestion holds

Textmetadata
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.