Articles

The role of DNA damage and oxidative stress in radiation-induced heart disease

  • LIU Likun ,
  • OUYANG Weiwei ,
  • SU Shengfa ,
  • MA Zhu ,
  • LI Qingsong ,
  • WANG Yu ,
  • LUO Daxian ,
  • HE Zhixu ,
  • LU Bing
Expand
  • 1. Department of Thoracic Oncology, Affiliated Hospital, Guizhou Medical College, Guiyang 550004, China;
    2. Teaching and Researching Section of Oncology, Guizhou Medical University, Guiyang 550001, China;
    3. Tissue Engineering and Stem Cell Research Center, Guizhou Medical University, Guiyang 550001, China

Received date: 2016-09-14

  Revised date: 2016-12-20

  Online published: 2017-02-28

Abstract

The radiation-induced heart disease (RIHD) is a progressive disorder induced by radiation, which may take years or decades to manifest. It can affect various structures of the heart, with a series of cardiac complications. In recent years, it is reported that the heart damage caused by the conventional chest radiotherapy, especially the delayed type of myocardial injuries becomes very serious under the control of the normal tissue tolerance dose. The RIHD can increase the heart stiffness, decrease the myocardial systolic and diastolic functions, resulting in the myocardial electrophysiological dysfunction, the arrhythmia, the heart failure and the sudden death. At present, there is still a lack of effective treatment for the RIHD, the basic reason is that the causes and pathogenesis of the RIHD promoted chronic heart failure from early asymptomatic condition have not been fully clarified. This paper reviews the role of the DNA damage and the oxidative stress in the RIHD to help the prevention and treatment of the RIHD.

Cite this article

LIU Likun , OUYANG Weiwei , SU Shengfa , MA Zhu , LI Qingsong , WANG Yu , LUO Daxian , HE Zhixu , LU Bing . The role of DNA damage and oxidative stress in radiation-induced heart disease[J]. Science & Technology Review, 2017 , 35(4) : 74 -78 . DOI: 10.3981/j.issn.1000-7857.2017.04.013

References

[1] Taylor C W, Povall J M, McGale P, et al. Cardiac dose from tangential breast cancer radiotherapy in the year 2006[J]. International Journal of Radiation Oncology Biology Physics, 2008, 72(2):501-507.
[2] Mulrooney D A, Yeazel M W, Kawashima T, et al. Cardiac outcomes in a cohort of adult survivors of childhood and adolescent cancer:retro-spective analysis of the Childhood Cancer Survivor Study cohort[J]. The BMJ, 2009, 339:b4606.
[3] Swerdlow A J, Higgins C D, Smith P, et al. Myocardial infarction mor-tality risk after treatment for Hodgkin disease:A collaborative British cohort study[J]. Journal of National Cancer Institute, 2007, 99(3):206-214.
[4] Galper S L, Yu J B, Mauch P M, et al. Clinically significant cardiac dis-ease in patients with Hodgkin lymphoma treated with mediastinal irradi-ation[J]. Blood, 2011, 117(2):412-418.
[5] Tukenova M, Guibout C, Oberlin O, et al. Role of cancer treatment in long-term overall and cardiovascular mortality after childhood cancer[J]. Journal of Clinical Oncology, 2010, 28(8):1308-1315.
[6] Laflamme M A, Murry C E. Heart regeneration[J]. Nature, 2011, 473(7347):326-335.
[7] Puente B N, Kimura W, Muralidhar S A, et al. The oxygen-rich postna-tal environment induces cardiomyocyte cell-cycle arrest through DNA damage response[J]. Cell, 2014, 157(3):565-579.
[8] Nikjoo H. Track structure in radiation biology:Theory and applications[J]. International Journal of Radiation Biology, 1998, 73(4):355-364.
[9] Asaithamby A, Chen D J. Mechanism of cluster DNA damage repair in response to high-atomic number and energy particles radiation[J]. Muta-tion Research, 2011, 711(1-2):87-99.
[10] Asaithamby A. Repair of HZE-particle-induced DNA double-strand breaks in normal human fibroblasts[J]. Radiation Research, 2008, 169(4):437-446.
[11] Zhang Z L, Bai Z H, Wang X B, et al. miR-186 and 326 predict the prognosis of pancreatic ductal adenocarcinoma and affect the prolifera-tion and migration of cancer cells[J]. Public Liblary of Science, 2015, 10(3):e0118814.
[12] Firsanov D, Vasilishina A, Kropotov A, et al. Dynamics of gammaH2AX formation and elimination in mammalian cells after X-irradiation[J]. Biochimie, 2012, 94(11):2416-2422.
[13] Salata C, Ferreira-Machado S C, De Andrade C B, et al. Apoptosis in-duction of cardiomyocytes and subsequent fibrosis after irradiation and neoadjuvant chemotherapy[J]. International Journal of Radiation Biology, 2014, 90(4):284-290.
[14] Lee C L, Moding E J, Cuneo K C, et al. p53 functions in endothelial cells to prevent radiation-induced myocardial injury in mice[J]. Sci-ence Signaling, 2012, 5(234):ra52.
[15] Mitchel R E, Hasu M, Bugden M, et al. Low-dose radiation exposure and protection against atherosclerosis in ApoE-/-mice:The influence of P53 heterozygosity[J]. Radiation Research, 2013, 179(2):190-199.
[16] Chen Y R, Zweier J L. Cardiac mitochondria and reactive oxygen spe-cies generation[J]. Circulation Research, 2014, 114(3):524-537.
[17] Li Y, Wang X Y, Zhang Z L, et al. Excess ROS induced by AAPH causes myocardial hypertrophy in the developing chick embryo[J]. In-ternational Journal of Cardiology, 2014, 176(1):62-73.
[18] Bloom W, Zirkle R E, Uretz R B. Irradiation of parts of individual cells. III. Effects of chromosomal and extrachromosomal irradiation on chromosome movements[J]. Annals of the New York Academy Scienc-es, 1955, 59(4):503-513.
[19] Zhou H, Hong M, Chai Y, et al. Consequences of cytoplasmic irradia-tion:studies from microbeam[J]. Journal of Radiation Research, 2009, 50(Suppl A):A59-A65.
[20] Kulkarni R, Marples B, Balasubramaniam M, et al. Mitochondrial gene expression changes in normal and mitochondrial mutant cells af-ter exposure to ionizing radiation[J]. Radiation Research, 2010, 173(5):635-644.
[21] Piquereau J, Caffin F, Novotova M, et al. Mitochondrial dynamics in the adult cardiomyocytes:which roles for a highly specialized cell?[J]. Frontiers in Physiology, 2003, 4:102.
[22] Chen K, Keaney J F J r. Evolving concepts of oxidative stress and re-active oxygen species in cardiovascular disease[J]. Current Atheroscle-rosis Reports, 2012, 14(5):476-483.
[23] Genova M L, Pich M M, Bernacchia A. The mitochondrial production of reactive oxygen species in relation to aging and pathology[J]. An-nals of the New York Academy of Sciences, 2004, 1011(4):86-100.
[24] Indo H P, Inanami O, Koumura T, et al. Roles of mitochondria-gener-ated reactive oxygen species on X-ray-induced apoptosis in a human hepatocellular carcinoma cell line[J]. Free Radical Research, 2012, 46(8):1029-1043.
[25] Ogura A, Oowada S, Kon Y, et al. Redox regulation in radiation-in-duced cytochrome c release from mitochondria of human lung carcino-ma A549 cells[J]. Cancer Letters, 2009, 277(1):64-71.
[26] Kobashigawa S, Suzuki K, Yamashita S. Ionizing radiation accelerates Drp1-dependent mitochondrial fission:Which involves delayed mito-chondrial reactive oxygen species production in normal human fibro-blast-like cells[J]. Biochemical and Biophys Research Communica-tions, 2011, 414(4):795-800.
[27] Zorov D B, Juhaszova M, Sollott S J. Mitochondrial ROS-induced ROS release:An update and review[J]. Biochimica et Biophysica Ccta, 2006, 1757(5-6):509-517.
[28] Zorov D B, Filburn C R, Klotz L O, et al. Reactive oxygen species (ROS)-induced ROS release:A new phenomenon accompanying induc-tion of the mitochondrial permeability transition in cardiac myocytes[J]. Journal of Experimental Medicine, 2000, 192(7):1001-1014.
[29] Canseco D C, Kimura W K, Garg S, et al. Human ventricular unload-ing induces cardiomyocyte proliferation[J]. Journal of the American College of Cardiology, 2015, 65(9):892-900.
[30] Senyo S E, Steinhauser M L, Pizzimenti C L, et al. Mammalian heart renewal by pre-existing cardiomyocytes[J]. Nature, 2013, 493(7432):433-436.
[31] Ali S R, Hippenmeyer S, Saadat L V, et al. Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice[J]. PNAS, 2014, 111(24):8850-8855.
[32] Kimura W, Xiao F, Canseco D C, et al. Hypoxia fate mapping identi-fies cycling cardiomyocytes in the adult heart[J]. Nature, 2015, 523(7559):226-230.
Outlines

/