Abstract
Radiotherapy of thoracic and chest wall tumors, if all or part of the heart was included in the radiation field, can lead to radiation-induced heart disease (RIHD), a late and potentially severe side effect. RIHD presents clinically several years after irradiation and manifestations include accelerated atherosclerosis, pericardial and myocardial fibrosis, conduction abnormalities, and injury to cardiac valves. The pathogenesis of RIHD is largely unknown, and a treatment is not available. Hence, ongoing pre-clinical studies aim to elucidate molecular and cellular mechanisms of RIHD. Here, an overview of recent pre-clinical studies is given, and based on the results of these studies, potential targets for intervention in RIHD are discussed.
Keywords: Radiation, heart, animal models, transforming growth factor-beta, renin-angiotensin system, mast cells, endothelin system, sensory nerves, models, transforming, angiotensin, endothelin, sensory, (RIHD), atherosclerosis, pericardial, myocardial fibrosis, pathogenesis, (myocardial necrosis, (PET), (SPECT), (RAS), Endothelial dysfunction, chemokines, TGF-β, mRNA, (Ang II), ACE, Captopril, (Ws), (CGRP), (TNF-α), IGF-1, (MMP), ETA, ETB
Current Drug Targets
Title: Potential Targets for Intervention in Radiation-Induced Heart Disease
Volume: 11 Issue: 11
Author(s): M. Boerma and M. Hauer-Jensen
Affiliation:
Keywords: Radiation, heart, animal models, transforming growth factor-beta, renin-angiotensin system, mast cells, endothelin system, sensory nerves, models, transforming, angiotensin, endothelin, sensory, (RIHD), atherosclerosis, pericardial, myocardial fibrosis, pathogenesis, (myocardial necrosis, (PET), (SPECT), (RAS), Endothelial dysfunction, chemokines, TGF-β, mRNA, (Ang II), ACE, Captopril, (Ws), (CGRP), (TNF-α), IGF-1, (MMP), ETA, ETB
Abstract: Radiotherapy of thoracic and chest wall tumors, if all or part of the heart was included in the radiation field, can lead to radiation-induced heart disease (RIHD), a late and potentially severe side effect. RIHD presents clinically several years after irradiation and manifestations include accelerated atherosclerosis, pericardial and myocardial fibrosis, conduction abnormalities, and injury to cardiac valves. The pathogenesis of RIHD is largely unknown, and a treatment is not available. Hence, ongoing pre-clinical studies aim to elucidate molecular and cellular mechanisms of RIHD. Here, an overview of recent pre-clinical studies is given, and based on the results of these studies, potential targets for intervention in RIHD are discussed.
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Cite this article as:
Boerma M. and Hauer-Jensen M., Potential Targets for Intervention in Radiation-Induced Heart Disease, Current Drug Targets 2010; 11 (11) . https://dx.doi.org/10.2174/1389450111009011405
DOI https://dx.doi.org/10.2174/1389450111009011405 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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