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人环素心脏毒性的初始阶段涉及心脏纤维细胞激活和代谢开关

Marialucia Telesca¹, Maria Donniacuo¹, Gabriella Bellocchio¹

¹Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", Via Costantinopoli 16, 80138 Naples, Italy.

|January 11, 2024

概括

多克索鲁比 (DOX) 通过激活心脏纤维细胞 (CFs) 导致早期心脏功能障碍. 这种在CF中导致纤维化的代谢开关,在心脏损伤之前发生,并为antracycline心肌病提供了一个新的治疗点.

科学领域:

心脏病学心脏病学
在瘤学瘤学.
生物化学生物化学

背景情况:

doxorubicin (DOX) 治疗可能会导致心脏毒性,最初表现为腹功能障碍.
潜在的机制,特别是早期心脏纤维细胞 (CF) 激活和纤维化,仍然不清楚.

研究的目的:

为了调查CF激活是否先于DOX诱导的心肌功能障碍.
评估DOX对CF代谢和表型的影响.

主要方法:

从DOX注射后的老鼠和在体外暴露于DOX的天真CF中分离出CF.
通过氧气消耗率和细胞外酸化来评估细胞代谢.
分析了CF表型和亲纤维菌标记物.

主要成果:

DOX诱导了早期的透缩功能障碍,并保留了喷射分数.
在DOX暴露后立即观察到亲纤维重塑和CF转变.
DOX触发了CF代谢活动的增加和向糖解转移,在体内和体外都是一致的.

结论:

由DOX诱导的代谢重编程和CFs的激活预测心肌损伤.
这种早期的CF激活和代谢切换代表了预防antracycline心肌病的潜在治疗标.

关键词:

的心脏纤维细胞.心脏有毒性心脏有毒性现型开关现型开关现型开关文本 doxorubicin 的使用情况.

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