化疗药物所致心脏毒性的防治研究进展

doi:10.19586/j.2095-2341.2026.0008

生物技术进展 ›› 2026, Vol. 16 ›› Issue (2): 348-355.DOI: 10.19586/j.2095-2341.2026.0008

• 进展评述 • 上一篇

化疗药物所致心脏毒性的防治研究进展

陈炎(), 刘治达

哈尔滨商业大学药学院，哈尔滨 150076

收稿日期:2026-01-14 接受日期:2026-02-27 出版日期:2026-03-25 发布日期:2026-04-27
作者简介:陈炎 E-mail: 1028560410@qq.com

Research Progress on the Prevention and Treatment of Cardiotoxicity Caused by Chemotherapy Drugs

Yan CHEN(), Zhida LIU

School of Pharmacy，Harbin University of Commerce，Harbin 150076，China

Received:2026-01-14 Accepted:2026-02-27 Online:2026-03-25 Published:2026-04-27

摘要/Abstract

摘要：

随着抗肿瘤治疗方法的不断创新与发展，肿瘤患者预后显著改善，然而化疗药物所致的心脏毒性问题日益凸显。这种毒性反应不仅严重限制了肿瘤患者的治疗方案选择，也对其生存质量及长期预后构成重要影响。系统归纳了常见化疗药物相关心脏毒性的临床表现及其作用机制，综述了国内外在预防与治疗方面的研究进展，梳理了现有的常见及新型防治策略，以期为临床应对化疗药物心脏毒性提供理论参考与实践依据。

关键词: 化疗药物, 心脏毒性, 致病机制, 新型策略

Abstract:

With the continuous innovation and development of anti-tumor treatment methods， the prognosis of cancer patients has been significantly improved. However， the problem of cardiotoxicity induced by chemotherapeutic drugs has become increasingly prominent. This toxic reaction not only severely limits the choice of treatment regimens for cancer patients but also exerts an important impact on their quality of life and long-term prognosis. This article systematically summarized the clinical manifestations and action mechanisms of cardiotoxicity associated with common chemotherapeutic drugs， reviewed the research progress in prevention and treatment at home and abroad， and sorted out the existing common and new prevention and treatment strategies， in order to provide theoretical reference and practical basis for the clinical management of chemotherapy-induced cardiotoxicity.

Key words: chemotherapy drugs, cardiotoxicity, pathogenesis, novel strategy

中图分类号:

Q819

陈炎, 刘治达. 化疗药物所致心脏毒性的防治研究进展[J]. 生物技术进展, 2026, 16(2): 348-355.

Yan CHEN, Zhida LIU. Research Progress on the Prevention and Treatment of Cardiotoxicity Caused by Chemotherapy Drugs[J]. Current Biotechnology, 2026, 16(2): 348-355.

图/表 1

参考文献 72

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常见化疗药物类型	化疗药物名称	心脏毒性作用	分子机制
蒽环类药物	阿霉素、柔红霉素、表柔比星和伊达比星等	心肌细胞死亡；左心室功能障碍，最终降低心排血量^[7]	活性氧（reactive oxygen species，ROS）的生成与自身抗氧化作用的失衡^[8]；由拓扑异构酶Ⅱ与肿瘤结合引起的DNA双链裂解^[9]；细胞内钙超载^[10]； miRNA表达的上调损害心肌细胞线粒体^[11]；促进释放炎症因子^[12]；转化生长因子β信号的增强和肌成纤维细胞的激活^[13]
烷基化试剂	环磷酰胺	程序性细胞凋亡，导致心脏应激和心力衰竭^[14]	环磷酰胺在肝脏分解后产生的丙烯酰胺损害心肌细胞和内皮细胞；降低抗氧化剂的水平，导致心肌细胞中脂肪酸氧化的下调^[15]
铂类药物	顺铂	导致心肌细胞和血管内皮细胞受损，进而引起心肌细胞收缩功能障碍^[16]	扰乱细胞内氧化应激和抗氧化应激的平衡，导致氧自由基增加、DNA损伤和细胞凋亡^[17]
紫杉烷类	紫杉醇、多西他赛	轻度心肌损伤，表现为QT间期延长，心动过缓及心房心室纤维性颤动^[18]	促进微管蛋白聚合并抑制解聚，从而抑制肿瘤细胞形成纺锤体，进一步抑制有丝分裂进程，导致细胞周期停滞，抑制细胞增殖^[19]
代谢拮抗物	5-氟尿嘧啶、卡培他滨、替吉奥、TAS-102等	大部分可逆，导致冠状动脉血管痉挛和血管收缩^[20]	NO合成的改变；活性氧物质积累导致的心肌细胞凋亡^[21]；蛋白激酶C引起不依赖内皮的血管收缩^[22]；血浆内皮素-1水平升高^[23]

常见化疗药物类型	化疗药物名称	心脏毒性作用	分子机制
蒽环类药物	阿霉素、柔红霉素、表柔比星和伊达比星等	心肌细胞死亡；左心室功能障碍，最终降低心排血量^[7]	活性氧（reactive oxygen species，ROS）的生成与自身抗氧化作用的失衡^[8]；由拓扑异构酶Ⅱ与肿瘤结合引起的DNA双链裂解^[9]；细胞内钙超载^[10]； miRNA表达的上调损害心肌细胞线粒体^[11]；促进释放炎症因子^[12]；转化生长因子β信号的增强和肌成纤维细胞的激活^[13]
烷基化试剂	环磷酰胺	程序性细胞凋亡，导致心脏应激和心力衰竭^[14]	环磷酰胺在肝脏分解后产生的丙烯酰胺损害心肌细胞和内皮细胞；降低抗氧化剂的水平，导致心肌细胞中脂肪酸氧化的下调^[15]
铂类药物	顺铂	导致心肌细胞和血管内皮细胞受损，进而引起心肌细胞收缩功能障碍^[16]	扰乱细胞内氧化应激和抗氧化应激的平衡，导致氧自由基增加、DNA损伤和细胞凋亡^[17]
紫杉烷类	紫杉醇、多西他赛	轻度心肌损伤，表现为QT间期延长，心动过缓及心房心室纤维性颤动^[18]	促进微管蛋白聚合并抑制解聚，从而抑制肿瘤细胞形成纺锤体，进一步抑制有丝分裂进程，导致细胞周期停滞，抑制细胞增殖^[19]
代谢拮抗物	5-氟尿嘧啶、卡培他滨、替吉奥、TAS-102等	大部分可逆，导致冠状动脉血管痉挛和血管收缩^[20]	NO合成的改变；活性氧物质积累导致的心肌细胞凋亡^[21]；蛋白激酶C引起不依赖内皮的血管收缩^[22]；血浆内皮素-1水平升高^[23]

化疗药物所致心脏毒性的防治研究进展

Research Progress on the Prevention and Treatment of Cardiotoxicity Caused by Chemotherapy Drugs

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[1]	安外尔·约麦尔阿卜拉, 布尔兰·叶尔肯别克, 孙莉莉, 刘富中, 迪丽娜尔·叶尔夏提, 郭文佳. 基于m5C相关基因构建三阴性乳腺癌预后预测模型及药物敏感性分析[J]. 生物技术进展, 2024, 14(1): 149-159.
[2]	姜辉,,刘玉琴,. 结核病合并糖尿病的流行现状及其防控[J]. 生物技术进展, 2017, 7(1): 25-29.