Evidence map›Paper›PMID 22174747›Full record

ArticlePloS one2011

Radiation-induced signaling results in mitochondrial impairment in mouse heart at 4 weeks after exposure to X-rays.

Zarko Barjaktarovic, Dominik Schmaltz, Alena Shyla, Omid Azimzadeh, Sabine Schulz, Julia Haagen, Wolfgang Dörr, Hakan Sarioglu, Alexander Schäfer, Michael J Atkinson and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
5.3field-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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
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  7. Application of stereotactic radiotherapy in the treatment of cardiovascular diseases through sympathectomy.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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  14. Cardiac radiotherapy transiently alters left ventricular electrical properties and induces cardiomyocyte-specific ventricular substrate changes in heart failure.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023
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21 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 1 country.

Zarko BarjaktarovicInstitute of Radiation Biology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. zarko.barjaktarovic@helmholtz-muenchen.de
Dominik Schmaltz
Alena Shyla
Omid Azimzadeh
Sabine Schulz
Julia Haagen
Wolfgang Dörr
Hakan Sarioglu
Alexander Schäfer
Michael J Atkinson
Hans Zischka
Soile Tapio
Helmholtz Zentrum München · DEUniversity Hospital Carl Gustav Carus · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRadiation therapy treatment of breast cancer, Hodgkin's disease or childhood cancers expose the heart to high local radiation doses, causing an increased risk of cardiovascular disease in the survivors decades after the treatment. The mechanisms that underlie the radiation damage remain poorly understood so far. Previous data show that impairment of mitochondrial oxidative metabolism is directly linked to the development of cardiovascular disease. METHODOLOGY/PRINCIPAL

findingsIn this study, the radiation-induced in vivo effects on cardiac mitochondrial proteome and function were investigated. C57BL/6N mice were exposed to local irradiation of the heart with doses of 0.2 Gy or 2 Gy (X-ray, 200 kV) at the age of eight weeks, the control mice were sham-irradiated. After four weeks the cardiac mitochondria were isolated and tested for proteomic and functional alterations. Two complementary proteomics approaches using both peptide and protein quantification strategies showed radiation-induced deregulation of 25 proteins in total. Three main biological categories were affected: the oxidative phophorylation, the pyruvate metabolism, and the cytoskeletal structure. The mitochondria exposed to high-dose irradiation showed functional impairment reflected as partial deactivation of Complex I (32%) and Complex III (11%), decreased succinate-driven respiratory capacity (13%), increased level of reactive oxygen species and enhanced oxidation of mitochondrial proteins. The changes in the pyruvate metabolism and structural proteins were seen with both low and high radiation doses. CONCLUSION/SIGNIFICANCE: This is the first study showing the biological alterations in the murine heart mitochondria several weeks after the exposure to low- and high-dose of ionizing radiation. Our results show that doses, equivalent to a single dose in radiotherapy, cause long-lasting changes in mitochondrial oxidative metabolism and mitochondria-associated cytoskeleton. This prompts us to propose that these first pathological changes lead to an increased risk of cardiovascular disease after radiation exposure.

Indexed as

AnimalsComputational BiologyCytochromes c1Dose-Response Relationship, RadiationElectron Transport Complex IElectron Transport Complex IIIElectrophoresis, Gel, Two-DimensionalImmunoblottingMiceMice, Inbred C57BLMitochondriaMitochondrial ProteinsMyocardiumOxidation-ReductionPhosphorylationProteomicsCytochromes c1Electron Transport Complex IElectron Transport Complex IIIMitochondrial ProteinsReactive Nitrogen SpeciesReactive Oxygen SpeciesSuccinic Acid

Identifiers

PMID22174747
PMCPMC3234240
OpenAlexW1964113973

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.