Evidence map›Paper›PMID 30764828›Full record

ReviewRespiratory research2019

Is cellular senescence involved in cystic fibrosis?

Valentino Bezzerri, Francesco Piacenza, Nicole Caporelli, Marco Malavolta, Mauro Provinciali, Marco Cipolli

Open access · goldAbstract readReview
In one paragraph

Review in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Senotherapy for chronic lung disease.Pharmacological reviews · 2025
    Review
  5. The ageing of people living with cystic fibrosis: what to expect now?European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  6. Article
  7. Cellular Senescence Contributes to the Progression of Hyperoxic Bronchopulmonary Dysplasia.American journal of respiratory cell and molecular biology · 2024
    Article
  8. Article
  9. Impact ofInternational journal of molecular sciences · 2022
    Review
  10. Article
  11. Inflammaging and Cannabinoids.Ageing research reviews · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Enhancing Cystic Fibrosis Immune Regulation.Frontiers in pharmacology · 2021
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  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

6 authors at 3 institutions in 1 country.

Valentino BezzerriCystic Fibrosis Center, Azienda Ospedaliera Universitaria Ospedali Riuniti, 60121, Ancona, Italy.
Francesco PiacenzaAdvanced Technology Center for Aging Research, Scientific Technological Area, IRCCS INRCA, 60121, Ancona, Italy.
Nicole CaporelliCystic Fibrosis Center, Azienda Ospedaliera Universitaria Ospedali Riuniti, 60121, Ancona, Italy.
Marco MalavoltaAdvanced Technology Center for Aging Research, Scientific Technological Area, IRCCS INRCA, 60121, Ancona, Italy.
Mauro ProvincialiAdvanced Technology Center for Aging Research, Scientific Technological Area, IRCCS INRCA, 60121, Ancona, Italy.
Marco CipolliCystic Fibrosis Center, Azienda Ospedaliera Universitaria Ospedali Riuniti, 60121, Ancona, Italy. marco.cipolli@ospedaliriuniti.marche.it.
Azienda Ospedaliero Universitaria Ospedali Riuniti · ITIstituto Nazionale di Riposo e Cura per Anziani · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary disease is the main cause of the morbidity and mortality of patients affected by cystic fibrosis (CF). The lung pathology is dominated by excessive recruitment of neutrophils followed by an exaggerated inflammatory process that has also been reported to occur in the absence of apparent pathogenic infections. Airway surface dehydration and mucus accumulation are the driving forces of this process. The continuous release of reactive oxygen species and proteases by neutrophils contributes to tissue damage, which eventually leads to respiratory insufficiency. CF has been considered a paediatric problem for several decades. Nevertheless, during the last 40 years, therapeutic options for CF have been greatly improved, turning CF into a chronic disease and extending the life expectancy of patients. Unfortunately, chronic inflammatory processes, which are characterized by a substantial release of cytokines and chemokines, along with ROS and proteases, can accelerate cellular senescence, leading to further complications in adulthood. The alterations and mechanisms downstream of CFTR functional defects that can stimulate cellular senescence remain unclear. However, while there are correlative data suggesting that cellular senescence may be implicated in CF, a causal or consequential relationship between cellular senescence and CF is still far from being established. Senescence can be both beneficial and detrimental. Senescence may suppress bacterial infections and cooperate with tissue repair. Additionally, it may act as an effective anticancer mechanism. However, it may also promote a pro-inflammatory environment, thereby damaging tissues and leading to chronic age-related diseases. In this review, we present the most current knowledge on cellular senescence and contextualize its possible involvement in CF.

Indexed as

Cellular SenescenceCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorHumansCystic Fibrosis Transmembrane Conductance RegulatorCellular senescenceCystic fibrosisSASP

Identifiers

PMID30764828
PMCPMC6376730
OpenAlexW2911465360

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.