Evidence map›Paper›PMID 30965013›Full record

ReviewAmerican journal of respiratory cell and molecular biology2019

Cellular Senescence: The Trojan Horse in Chronic Lung Diseases.

Shruthi Hamsanathan, Jonathan K Alder, Jacobo Sellares, Mauricio Rojas, Aditi U Gurkar, Ana L Mora

Open access · greenAbstract readReview
In one paragraph

Review in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. IFN-Mediated Bronchial Epithelium Cellular Senescence in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025
    Article
  7. Article
  8. Review
  9. Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Senescence of lung mesenchymal stem cells of preterm infants by cyclic stretch and hyperoxia via p21.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  19. Review
  20. Article
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 5 institutions in 3 countries.

Shruthi Hamsanathan1 Aging Institute.
Jonathan K Alder2 Division of Pulmonary Allergy and Critical Care Medicine, and.ORCID 0000-0003-3741-6512
Jacobo Sellares4 Interstitial Lung Disease Program, Servei de Pneumologia, Hospital Clínic Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Mauricio Rojas2 Division of Pulmonary Allergy and Critical Care Medicine, and.ORCID 0000-0001-7340-4784
Aditi U Gurkar1 Aging Institute.ORCID 0000-0003-4338-0624
Ana L Mora1 Aging Institute.ORCID 0000-0003-1653-8318
Pulmonary and Allergy Associates · USGeriatric Research Education and Clinical Center · USInstitute of Aging · CAInstituto de Salud Carlos III · ESUniversity of Pittsburgh · US

Funding

Mechanisms of Telomere-Mediated Lung DiseaseR01HL135062 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jonathan K. Alder · 2018 to 2026
$4.1M
Aging of Mesenchymal Stem Cells Missing Link in IPFR01HL123766 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROJAS, MAURICIO · 2015 to 2018
$1.9M
Signaling mechanisms by which mitochondria regulates fibrosis in the lungR01HL131789 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MORA, ANA LUCIA · 2016 to 2019
$1.7M
Modulators of DNA damage associated nucleo-mitochondrial communication in agingR00AG049126 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GURKAR, ADITI U · 2017 to 2019
$835k
Mechanisms of Teleomere-Mediated EmphysemaR00HL113105 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ALDER, JONATHAN K. · 2014 to 2016
$743k
NHLBI NIH HHS R00 HL113105NHLBI NIH HHS R01 HL123766NHLBI NIH HHS R01 HL131789NHLBI NIH HHS R01 HL135062NIA NIH HHS R00 AG049126
6 · The paper itself

Abstract

Senescence is a cell fate decision characterized by irreversible arrest of proliferation accompanied by a senescence-associated secretory phenotype. Traditionally, cellular senescence has been recognized as a beneficial physiological mechanism during development and wound healing and in tumor suppression. However, in recent years, evidence of negative consequences of cellular senescence has emerged, illuminating its role in several chronic pathologies. In this context, senescent cells persist or accumulate and have detrimental consequences. In this review, we discuss the possibility that in chronic obstructive pulmonary disease, persistent senescence impairs wound healing in the lung caused by secretion of proinflammatory senescence-associated secretory phenotype factors and exhaustion of progenitor cells. In contrast, in idiopathic pulmonary fibrosis, chronic senescence in alveolar epithelial cells exacerbates the accumulation of senescent fibroblasts together with production of extracellular matrix. We review how cellular senescence may contribute to lung disease pathology.

Indexed as

Cellular SenescenceWound HealingAlveolar Epithelial CellsChronic DiseaseFibroblastsHumansIdiopathic Pulmonary FibrosisPulmonary Disease, Chronic Obstructivechronic obstructive pulmonary diseaseidiopathic pulmonary fibrosislungsenescencesenescence-associated secretory phenotype

Identifiers

PMID30965013
PMCPMC6604222
OpenAlexW2935979948

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.