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细胞外矩阵重塑的时间动力学在人环素诱导的心脏毒性

Fibi Meshrkey¹, Somaya Y Ibrahim^2,3, Rushita A Bagchi^3,4

¹Ralph E. Martin Department of Chemical Engineering, University of Arkansas, Fayetteville, AR 72701, USA.

|September 26, 2025

概括

人环素化疗会引起心脏损伤,主要是通过心脏纤维细胞 (CFs). 这些细胞促进纤维化和炎症,导致心脏功能障碍和失败,即使在治疗后数年.

科学领域:

心脏病学心脏病学
在瘤学瘤学.
纤维化研究纤维化研究

背景情况:

人环素是重要的化疗药物,但会引起剂量依赖的心脏毒性.
传统上,心脏毒性与直接心肌细胞损伤有关.
新兴研究涉及心脏纤维细胞 (CFs) 在人马环素心脏毒性.

研究的目的:

审查心脏纤维细胞在人环素诱导心脏毒性的作用.
为了检查多克索鲁比对CF在不同伤害阶段的影响.
为了突出CFs对纤维化,衰老和炎症的贡献.

主要方法:

文献综述侧重于人环素,多克索鲁比辛 (DOX) 和心脏纤维细胞.
对DOX对CF和细胞外矩阵重塑的影响的分析.
检查人类循环素心脏毒性的时间方面.

主要成果:

DOX激活CFs,促进细胞外基质重塑和纤维化.
CF诱导的衰老和原生成加剧了心肌炎症和功能障碍.
环素心脏毒性呈现为急性,亚急性或慢性,晚期损伤通常是不可逆转的.

结论:

心脏纤维细胞在人环素心脏毒性中起着至关重要的作用.
了解CF机制提供了潜在的治疗点.
预防或减轻CF激活可以保护心脏免受化疗损伤.

关键词:

环素是一种环素.心脏毒性心脏毒性德克索鲁比辛 (doxorubicin) 是一种药物.细胞外的矩阵.纤维化纤维化

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