Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
Key Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.
Oxid Med Cell Longev. 2020 Oct 13;2020:4894625. doi: 10.1155/2020/4894625. eCollection 2020.
Recent therapeutic advances have significantly improved the short- and long-term survival rates in patients with heart disease and cancer. Survival in cancer patients may, however, be accompanied by disadvantages, namely, increased rates of cardiovascular events. Chemotherapy-related cardiac dysfunction is an important side effect of anticancer therapy. While advances in cancer treatment have increased patient survival, treatments are associated with cardiovascular complications, including heart failure (HF), arrhythmias, cardiac ischemia, valve disease, pericarditis, and fibrosis of the pericardium and myocardium. The molecular mechanisms of cardiotoxicity caused by cancer treatment have not yet been elucidated, and they may be both varied and complex. By identifying the functional genetic variations responsible for this toxicity, we may be able to improve our understanding of the potential mechanisms and pathways of treatment, paving the way for the development of new therapies to target these toxicities. Data from studies on genetic defects and pharmacological interventions have suggested that many molecules, primarily those regulating oxidative stress, inflammation, autophagy, apoptosis, and metabolism, contribute to the pathogenesis of cardiotoxicity induced by cancer treatment. Here, we review the progress of genetic research in illuminating the molecular mechanisms of cancer treatment-mediated cardiotoxicity and provide insights for the research and development of new therapies to treat or even prevent cardiotoxicity in patients undergoing cancer treatment. The current evidence is not clear about the role of pharmacogenomic screening of susceptible genes. Further studies need to done in chemotherapy-induced cardiotoxicity.
近年来，治疗方法的进步显著提高了心脏病和癌症患者的短期和长期生存率。然而，癌症患者的生存可能伴随着一些不利因素，即心血管事件发生率的增加。化疗相关的心脏功能障碍是癌症治疗的一个重要副作用。虽然癌症治疗的进步提高了患者的生存率，但治疗方法与心血管并发症有关，包括心力衰竭 (HF)、心律失常、心肌缺血、瓣膜疾病、心包炎和心包及心肌纤维化。癌症治疗引起的心脏毒性的分子机制尚未阐明，它们可能既有多样性又有复杂性。通过确定导致这种毒性的功能性遗传变异，我们也许能够更好地理解潜在的治疗机制和途径，为开发针对这些毒性的新疗法铺平道路。遗传缺陷和药物干预研究的数据表明，许多分子，主要是那些调节氧化应激、炎症、自噬、细胞凋亡和代谢的分子，有助于阐明癌症治疗引起的心脏毒性的发病机制。在这里，我们回顾了遗传研究在阐明癌症治疗介导的心脏毒性的分子机制方面的进展，并为治疗甚至预防接受癌症治疗的患者的心脏毒性的新疗法的研究和开发提供了见解。目前，关于易感基因的药物基因组筛查的作用还没有明确的证据。需要进一步研究化疗诱导的心脏毒性。
