由BCR-ABL1氨酸激酶抑制剂诱导的心脏毒性的线粒体功能障碍 - 潜在的机制,检测,潜在的治疗方法
Sheng Sun1,2, Jiqiu Qin1, Wenhao Liao1
1Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Cardiovascular toxicology
|July 21, 2023
概括
用于慢性髓性白血病的BCR-ABL1氨酸激酶抑制剂 (TKIs) 可以通过破坏线粒体引起心脏毒性. 了解这些机制是最大限度地减少伤害和改善患者结果的关键.
科学领域:
- 在瘤学瘤学.
- 心脏病学 心脏病学
- 线粒体生物学 线粒体生物学
背景情况:
- BCR-ABL1 氨酸激酶抑制剂 (TKI) 转化慢性髓性白血病 (CML) 治疗.
- 线粒体对心脏健康至关重要,但BCR-ABL1 TKIs可以通过线粒体损伤诱导心脏毒性.
- 这对CML幸存者构成风险.
研究的目的:
- 审查BCR-ABL1 TKI的心脏毒性.
- 阐明TKI诱导的线粒体损伤的潜在机制.
- 为临床决策和心脏保护策略提供信息.
主要方法:
- 关于BCR-ABL1 TKI心脏毒性的文献综述.
- 机制的分析,包括内质网膜 (ER) 应激,线粒体应激和反应性氧物种 (ROS) 生产.
- 探索其他与激酶相关的潜在心脏毒性途径.
主要成果:
- BCR-ABL1 TKIs可以通过各种线粒体功能障碍途径导致心脏毒性.
- 关键机制包括ER压力,线粒体压力,线粒体呼吸功能受损和ROS产量增加.
- 其他激酶和未明确的因素也可能有所贡献.
结论:
- 线粒体功能障碍是BCR-ABL1TKI诱导的心脏毒性的核心.
- 改善TKI的检测和管理,以及以线粒体为重点的心脏保护,至关重要.
- 尽量减少心脏毒性将减少CML患者的不良影响.
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