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辐射性心脏病发病机制认识的新见解

New Insights into the Understanding of Mechanisms of Radiation-Induced Heart Disease.

作者信息

Wang Kai-Xuan, Ye Cong, Yang Xu, Ma Ping, Yan Chen, Luo Lan

机构信息

Xuzhou Key Laboratory of Laboratory Diagnostics, School of Medical Technology, Xuzhou Medical University, 209 Tongshan Road, Xuzhou City, Jiangsu Province, 221004, People's Republic of China.

Department of Laboratory Medicine, Affiliated Hospital of Xuzhou Medical University, Xuzhou City, Jiangsu Province, 221004, People's Republic of China.

出版信息

Curr Treat Options Oncol. 2023 Jan;24(1):12-29. doi: 10.1007/s11864-022-01041-4. Epub 2023 Jan 4.

Abstract

Cancer patients who receive high-dose thoracic radiotherapy may develop radiation-induced heart disease (RIHD). The clinical presentation of RIHD comprises coronary artery atherosclerosis, valvular disease, pericarditis, cardiomyopathy, and conduction defects. These complications have significantly reduced due to the improved radiotherapy techniques. However, such methods still could not avoid heart radiation exposure. Furthermore, people who received relatively low-dose radiation exposures have exhibited significantly elevated RIHD risks in cohort studies of atomic bomb survivors and occupational exposures. The increased potential in exposure to natural and artificial ionizing radiation sources has emphasized the necessity to understand the development of RIHD. The pathological processes of RIHD include endothelial dysfunction, inflammation, fibrosis, and hypertrophy. The underlying mechanisms may involve the changes in oxidative stress, DNA damage response, telomere erosion, mitochondrial dysfunction, epigenetic regulation, circulation factors, protein post-translational modification, and metabolites. This review will discuss the recent advances in the mechanisms of RIHD at cellular and molecular levels.

摘要

接受高剂量胸部放疗的癌症患者可能会患上放射性心脏病(RIHD)。RIHD的临床表现包括冠状动脉粥样硬化、瓣膜疾病、心包炎、心肌病和传导缺陷。由于放疗技术的改进,这些并发症已显著减少。然而,这些方法仍无法避免心脏受到辐射。此外,在原子弹幸存者和职业暴露的队列研究中,接受相对低剂量辐射暴露的人群患RIHD的风险显著升高。天然和人工电离辐射源暴露可能性的增加凸显了了解RIHD发病机制的必要性。RIHD的病理过程包括内皮功能障碍、炎症、纤维化和肥大。潜在机制可能涉及氧化应激、DNA损伤反应、端粒侵蚀、线粒体功能障碍、表观遗传调控、循环因子、蛋白质翻译后修饰和代谢产物的变化。本综述将讨论RIHD在细胞和分子水平机制方面的最新进展。

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