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Wnt10b通过MAPK调制保护心肌细胞免受多克索鲁比诱导的细胞死亡

Lei Chen¹, Stefano H Byer¹, Rachel Holder¹

¹Department of Cardiovascular Medicine, University of Kansas School of Medicine, Kansas City, KS, United States of America.

|October 19, 2023

概括

Wnt10b通过减少亡和改善线粒体功能来保护心脏细胞免受多克索鲁比损伤. 这一发现为缓解化疗引起的心脏毒性提供了潜在的策略.

科学领域:

心脏病学心脏病学
分子生物学分子生物学
在瘤学瘤学.

背景情况:

德克索鲁比化疗会引起心脏毒性,使患者的心脏功能下降.
Wnt信号通路对于心脏修复至关重要,并可能减轻多克索鲁比辛的作用.
了解Wnt的心脏保护机制对于癌症患者至关重要.

研究的目的:

研究Wnt10b对人类心肌细胞中多克索鲁比诱导的心脏毒性的保护作用.
阐明Wnt10b减轻多克索鲁比诱导的亡的分子机制.

主要方法:

人类心肌细胞AC16细胞被Wnt10b和多克索鲁比辛治疗.
用MTT,TUNEL和JC-1试验评估了细胞活力,细胞亡和线粒体膜稳定性.
使用特定的抑制剂研究了ERK1/2和p38通路的作用,并量化了caspase 3/7活性.

主要成果:

Wnt10b显著减少了多克索鲁比诱导的亡,从70.1%降至50.1%.
随着Wnt10b治疗,LDH释放和酶3/7表达减少,而线粒体膜稳定性增加.
Wnt10b调节了ERK1/2和p38活动,减少了p38和增加了ERK1/2.2.

结论:

Wnt10b显示出显著的心脏保护作用,防止多克索鲁比引起的心脏毒性.
该机制涉及通过调节p38和ERK1/2信号通路来保护线粒体.
Wnt10b代表了预防化疗相关心脏损伤的潜在治疗策略.

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