Evidence map›Paper›PMID 24052614›Full record

ArticleJournal of the National Cancer Institute2013

Role of type II pneumocyte senescence in radiation-induced lung fibrosis.

Deborah E Citrin, Uma Shankavaram, Jason A Horton, William Shield, Shuping Zhao, Hiroaki Asano, Ayla White, Anastasia Sowers, Angela Thetford, Eun Joo Chung

Open access · greenAbstract read
In one paragraph

Article in Journal of the National Cancer Institute, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

121 citing papers in PubMed, 163 citations in OpenAlex.

  1. Article
  2. Article
  3. Radiomitigators: Breakthroughs in Post-Radiation Recovery.Antioxidants (Basel, Switzerland) · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

61 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Deborah E CitrinAffiliations of authors: Radiation Oncology Branch (DEC, US, JAH, WS, SZ, HA, AY, EJC) and Radiation Biology Branch (AS, AT), Center for Cancer Research, National Institutes of Health, Bethesda, MD.
Uma Shankavaram
Jason A Horton
William Shield
Shuping Zhao
Hiroaki Asano
Ayla White
Anastasia Sowers
Angela Thetford
Eun Joo Chung
National Institutes of Health · US

Funding

Mechanisms of Normal Tissue Toxicity From IrradiationZIABC010850 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CITRIN, DEBORAH · 2009 to 2025
$19.4M
Intramural NIH HHS
6 · The paper itself

Abstract

backgroundRadiation is a commonly delivered therapeutic modality for cancer. The causes underlying the chronic, progressive nature of radiation injury in the lung are poorly understood.

methodsC57Bl/6NCr mice were exposed to thoracic irradiation (n = 3 per dose and time point for tissue collection). Microarray analysis of gene expression from irradiated murine lung was performed using one-way analysis of variance with post hoc Scheffe analysis. Senescence and type II airway epithelial cell (AECII) count were assayed in irradiated murine lung tissue (n = 3 per condition). Irradiated mice were treated with diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase (NOX), and fibrosis was assessed by collagen assays. All statistical tests were two-tailed.

resultsGene expression in lung tissue from mice irradiated to 17.5 Gy clustered with that of aged unirradiated mice. Only fibrogenic exposures led to AECII senescence (0 Gy: 0.66% ± 0.67%; 5 Gy: 4.5% ± 1.19%; 17.5 Gy: 18.7% ± 3.05; P = .007) and depletion (0 Gy: 2.89 per alveolus ± 0.26; 5 Gy: 2.41 ± 0.19; 17.5 Gy: 1.6 ± 0.14; P < .001) at 30 weeks. Treatment of irradiated mice with DPI for 16 weeks markedly reduced collagen accumulation (5×6 Gy: 57.26 μg/lung ± 9.91; 5×6 Gy ± DPI: 36.54μg/lung ± 4.39; P = .03) and AECII senescence (5×6 Gy: 37.61% ± 4.82%; 5×6 Gy ± DPI: 12.38% ± 2.78; P < .001).

conclusionsThese studies identify senescence as an important process in AECII in vivo and indicate that NOX is a critical mediator of radiation-induced AECII senescence and pulmonary fibrosis.

Indexed as

Cellular SenescenceAlveolar Epithelial CellsAnimalsCollagenDisease Models, AnimalDose-Response Relationship, RadiationGene Expression RegulationLungMiceMice, Inbred C57BLNADPH OxidasesOnium CompoundsPulmonary FibrosisTime FactorsTissue Array AnalysisCollagendiphenyleneiodoniumNADPH OxidasesOnium Compounds

Identifiers

PMID24052614
PMCPMC3787909
OpenAlexW2126557512

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.