Evidence map›Paper›PMID 27663762›Full record

ArticleInternational journal of radiation oncology, biology, physics2016

Mammalian Target of Rapamycin Inhibition With Rapamycin Mitigates Radiation-Induced Pulmonary Fibrosis in a Murine Model.

Eun Joo Chung, Anastasia Sowers, Angela Thetford, Grace McKay-Corkum, Su I Chung, James B Mitchell, Deborah E Citrin

Abstract read
In one paragraph

Article in International journal of radiation oncology, biology, physics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.1field-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

39 citing papers in PubMed, 62 citations in OpenAlex.

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  8. Cellular Senescence: A Troy Horse in Pulmonary Fibrosis.International journal of molecular sciences · 2023
    Review
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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

7 authors at 2 institutions in 1 country.

Eun Joo ChungRadiation Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland.
Anastasia SowersRadiation Biology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland.
Angela ThetfordRadiation Biology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland.
Grace McKay-CorkumRadiation Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland.
Su I ChungRadiation Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland.
James B MitchellRadiation Biology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland.
Deborah E CitrinRadiation Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland. Electronic address: citrind@mail.nih.gov.
Center for Cancer Research · USNational 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
Mechanisms of Normal Tissue ToxicityZ01BC010850 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CITRIN, DEBORAH · 2007 to 2008
$1.0M
Intramural NIH HHS Z01 BC010850
6 · The paper itself

Abstract

purposeRadiation-induced pulmonary fibrosis (RIPF) is a late toxicity of therapeutic radiation. Signaling of the mammalian target of rapamycin drives several processes implicated in RIPF, including inflammatory cytokine production, fibroblast proliferation, and epithelial senescence. We sought to determine if mammalian target of rapamycin inhibition with rapamycin would mitigate RIPF. METHODS AND MATERIALS: C57BL/6NCr mice received a diet formulated with rapamycin (14 mg/kg food) or a control diet 2 days before and continuing for 16 weeks after exposure to 5 daily fractions of 6 Gy of thoracic irradiation. Fibrosis was assessed with Masson trichrome staining and hydroxyproline assay. Cytokine expression was evaluated by quantitative real-time polymerase chain reaction. Senescence was assessed by staining for β-galactosidase activity.

resultsAdministration of rapamycin extended the median survival of irradiated mice compared with the control diet from 116 days to 156 days (P=.006, log-rank test). Treatment with rapamycin reduced hydroxyproline content compared with the control diet (irradiation plus vehicle, 45.9 ± 11.8 μg per lung; irradiation plus rapamycin, 21.4 ± 6.0 μg per lung; P=.001) and reduced visible fibrotic foci. Rapamycin treatment attenuated interleukin 1β and transforming growth factor β induction in irradiated lungs compared with the control diet. Type II pneumocyte senescence after irradiation was reduced with rapamycin treatment at 16 weeks (3-fold reduction at 16 weeks, P<.001).

conclusionsRapamycin protected against RIPF in a murine model. Rapamycin treatment reduced inflammatory cytokine expression, extracellular matrix production, and senescence in type II pneumocytes.

Indexed as

Alveolar Epithelial CellsAnimalsbeta-GalactosidaseCellular SenescenceExtracellular MatrixFemaleHydroxyprolineInterleukin-1betaLungMacrophagesMiceMice, Inbred C57BLRadiation PneumonitisRadiation-Protective AgentsRadiation ToleranceSirolimusbeta-GalactosidaseHydroxyprolineInterleukin-1betamTOR protein, mouseRadiation-Protective AgentsSirolimusTOR Serine-Threonine KinasesTransforming Growth Factor beta

Identifiers

PMID27663762
PMCPMC5089209
OpenAlexW2522865647

What OpenQuestion holds

Textmetadata
LicenceTDM
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.