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通过GSK-3α激活,通过Keap1/Nrf2/HO-1轴减轻多克索鲁比诱导的心肌病变

Hezlin Marzook¹, Omama I Dawuod¹, Abdul Khader Mohammed¹

¹Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates.

|March 11, 2026

概括

糖原合成酶激酶-3α (GSK-3α) 通过增强抗氧化防御和减少亡来保护心脏细胞免受多克索鲁比 (Dox) 损伤. 这表明GSK-3α是Dox诱导心肌病的潜在治疗点.

科学领域:

心脏病学心脏病学
分子生物学分子生物学
生物化学生物化学

背景情况:

德克索鲁比 (Dox) 化疗可以引起心肌病,其特征是氧化应激,线粒体功能障碍和心脏细胞的亡.
糖原合成酶激酶-3α (GSK-3α) 在Dox诱导的心肌细胞亡中的作用及其潜在的信号通路尚不清楚.

研究的目的:

研究GSK-3α在调节线粒体完整性,氧化还原平衡和Dox压力下的心肌细胞中Nrf2信号传递中的作用.
为了确定GSK-3α过度表达是否可以防止Dox诱导的心脏损伤.

主要方法:

人类心肌细胞被用Dox治疗,有或没有GSK-3α过度表达.
评估了线粒体功能,反应性氧物种 (ROS) 生成和细胞染色体-c (Cyt-c) 释放.
分析了Keap1/Nrf2/HO-1信号通路组件和Nrf2亚细胞定位.

主要成果:

过度表达GSK-3α显著降低了Dox诱导的线粒体功能障碍和亡.
GSK-3α增强了Nrf2的核转位,增加了抗氧化酶HO-1的表达.
观察到自活动增加和氧化和亡信号的缓解.

结论:

GSK-3α作为Keap1/Nrf2/HO-1抗氧化途径的新型调节剂.
GSK-3α在Dox治疗的心肌细胞中显示出抗亡作用,这表明它是Dox诱导心肌病的潜在治疗标.

关键词:

抗氧化剂是一种抗氧化剂.自自是一种自的过程.心脏有毒性 - 心脏有毒性德克索鲁比辛是一种多克索鲁比辛.这是GSK-3α.凯普1号码是什么意思 Nrf2 没有任何问题.

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