在慢性淋巴细胞白血病的发病过程中,氧化状态变化的作用
M V Osikov1,2, E A Korobkin3,4, A A Fedosov5
1South Ural State Medical University, Ministry of Health of the Russian Federation, Chelyabinsk, Russia. prof.osikov@yandex.ru.
Doklady. Biochemistry and biophysics
|October 31, 2024
概括
氧化应激是由活性氧物种驱动的,在慢性淋巴细胞白血病 (CLL) 病原和耐药性方面发挥着关键作用. 向氧化还原状态为CLL提供了新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
背景情况:
- 慢性淋巴细胞白血病 (CLL) 是一种CD5+B细胞恶性瘤,病因不明.
- 氧化应激与CLL细胞存活率和治疗耐药性有关.
- 降解毒素状态的改变在CLL病变发生过程中至关重要.
研究的目的:
- 审查当前关于氧化还原状态变化在CLL病变发生中的作用的数据.
- 分析氧化应激和抗氧化剂防御在CLL中的影响.
- 探索在CLL中准氧化还原通路的治疗影响.
主要方法:
- 2018-2023年间发表的综合文献综述研究.
- 在PubMed和社会科学引用指数数据库中进行的搜索.
- 专注于CLL的致病性和自由基氧化过程.
主要成果:
- 由于过多的活性氧物种和抗氧化防御功能受损,CLL表现出氧化应激.
- 关键的酶如超氧化物脱酶-2和谷氨过氧化酶是上调的,而酶是下调的.
- 红色素核因子-2 (NRF2) 途径通过调节抗氧化酶并促进细胞存活来调节氧化应激和药物治疗的耐药性.
- FOXO3a的激活增强了抗氧化酶的表达和自然杀手细胞的活性,有助于瘤细胞的存活.
结论:
- 排毒状态失调是CLL病变和进展的关键因素.
- 该NRF2通路是CLL细胞中抗性的关键调解者.
- 向氧化还原平衡,包括NRF2降解和NADPH-氨酸氧化还原酶-1激活,是新型CLL治疗的有前途的策略.
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