Pathology and biology of radiation-induced cardiac disease

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Abstract

Heart disease is the leading global cause of death. The risk for this disease is significantly increased in populations exposed to ionizing radiation, but the mechanisms are not fully elucidated yet. This review aims to gather and discuss the latest data about pathological and biological consequences in the radiation-exposed heart in a comprehensive manner. A better understanding of the molecular and cellular mechanisms underlying radiation-induced damage in heart tissue and cardiac vasculature will provide novel targets for therapeutic interventions. These may be valuable for individuals clinically or occupationally exposed to varying doses of ionizing radiation.

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Aging, Cellular Senescence, and Cancer

Judith Campisi (2013)

For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of function that characterizes degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) functions that allow them to develop into a lethal tumor. This review discusses the idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence. The senescence response is widely recognized as a potent tumor suppressive mechanism. However, recent evidence strengthens the idea that it also drives both degenerative and hyperplastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.

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Endothelial cell senescence in human atherosclerosis: role of telomere in endothelial dysfunction.

Tohru Minamino, Hideaki Miyauchi, Toshihiko Yoshida … (2002)

The functional changes associated with cellular senescence may be involved in human aging and age-related vascular disorders. We have shown the important role of telomere and telomerase in vascular cell senescence in vitro. Progressive telomere shortening in vivo has been observed in the regions susceptible to atherosclerosis, implying contributions to atherogenesis. However, whether senescent vascular cells are present in the vasculature and contribute to the pathogenesis of atherosclerosis remains unclear. Senescence-associated beta-galactosidase (beta-gal) activity was examined in the coronary arteries and the internal mammary arteries retrieved from autopsied individuals who had had ischemic heart diseases. Strong beta-gal stainings were observed in atherosclerotic lesions of the coronary arteries but not in the internal mammary arteries. An immunohistochemical analysis using anti-factor VIII antibody demonstrated that beta-gal stained cells are vascular endothelial cells. To determine whether endothelial cell senescence causes endothelial dysfunction, we induced senescence in human aortic endothelial cells (HAECs) by inhibiting telomere function and examined the expression of intercellular adhesion molecule (ICAM)-1 and endothelial nitric oxide synthase (eNOS) activity. Senescent HAECs exhibited increased ICAM-1 expression and decreased eNOS activity, both of which are alterations implicated in atherogenesis. In contrast, introduction of telomerase catalytic component significantly extended the life span and inhibited the functional alterations associated with senescence in HAECs. Vascular endothelial cells with senescence-associated phenotypes are present in human atherosclerotic lesions, and endothelial cell senescence induced by telomere shortening may contribute to atherogenesis.

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Radiation exposure and circulatory disease risk: Hiroshima and Nagasaki atomic bomb survivor data, 1950-2003

Yukiko Shimizu, Kazunori Kodama, Nobuo Nishi … (2010)

Objective To investigate the degree to which ionising radiation confers risk of mortality from heart disease and stroke. Design Prospective cohort study with more than 50 years of follow-up. Setting Atomic bomb survivors in Hiroshima and Nagasaki, Japan. Participants 86 611 Life Span Study cohort members with individually estimated radiation doses from 0 to >3 Gy (86% received <0.2 Gy). Main outcome measures Mortality from stroke or heart disease as the underlying cause of death and dose-response relations with atomic bomb radiation. Results About 9600 participants died of stroke and 8400 died of heart disease between 1950 and 2003. For stroke, the estimated excess relative risk per gray was 9% (95% confidence interval 1% to 17%, P=0.02) on the basis of a linear dose-response model, but an indication of possible upward curvature suggested relatively little risk at low doses. For heart disease, the estimated excess relative risk per gray was 14% (6% to 23%, P<0.001); a linear model provided the best fit, suggesting excess risk even at lower doses. However, the dose-response effect over the restricted dose range of 0 to 0.5 Gy was not significant. Prospective data on smoking, alcohol intake, education, occupation, obesity, and diabetes had almost no impact on the radiation risk estimates for either stroke or heart disease, and misdiagnosis of cancers as circulatory diseases could not account for the associations seen. Conclusion Doses above 0.5 Gy are associated with an elevated risk of both stroke and heart disease, but the degree of risk at lower doses is unclear. Stroke and heart disease together account for about one third as many radiation associated excess deaths as do cancers among atomic bomb survivors.

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Journal

Journal ID (nlm-ta): J Radiat Res

Journal ID (iso-abbrev): J. Radiat. Res

Journal ID (publisher-id): jrr

Journal ID (hwp): jrr

Title: Journal of Radiation Research

Publisher: Oxford University Press

ISSN (Print): 0449-3060

ISSN (Electronic): 1349-9157

Publication date (Print): September 2016

Publication date (Electronic): 30 September 2016

Publication date PMC-release: 30 September 2016

Volume: 57

Issue: 5

Pages: 439-448

Affiliations

Helmholtz Zentrum München, German Research Center for Environmental Health GmbH, Institute of Radiation Biology, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany

Author notes

[* ]Corresponding author. Helmholtz Zentrum München, German Research Center for Environmental Health GmbH, Institute of Radiation Biology, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany. Tel: +49-89-3187-3445; Fax +49-89-3187-3378; Email: soile.tapio@ 123456helmholtz-muenchen.de

Article

Publisher ID: rrw064

DOI: 10.1093/jrr/rrw064

PMC ID: 5045085

PubMed ID: 27422929

SO-VID: 2295ef25-e24c-4e28-bae1-73d9ce4b1e52

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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@ 123456oup.com .

History

Date received : 18 February 2016

Date revision received : 04 April 2016

Date accepted : 09 May 2016

Page count

Pages: 10

Funding

Funded by: European Community's Seventh Framework Program (EURATOM);

Award ID: 295823

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Pathology and biology of radiation-induced cardiac disease

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Karger: Oncology

Most cited references 126

Aging, Cellular Senescence, and Cancer

Endothelial cell senescence in human atherosclerosis: role of telomere in endothelial dysfunction.

Radiation exposure and circulatory disease risk: Hiroshima and Nagasaki atomic bomb survivor data, 1950-2003

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