探索遗传变异在氧化应激易感性和疾病风险中的作用
S U Rehman1, J M Ashraf2, M M A Beg1
1ᵃAla-Too International University, Faculty of Medicine, Bishkek, Kyrgyzstan.
Brazilian journal of biology = Revista brasleira de biologia
|September 24, 2025
概括
遗传因素会影响对氧化应激的易感性,影响健康和疾病. 本综述详细介绍了抗氧化途径的遗传变异如何影响氧化应激和相关条件.
科学领域:
- 生物化学 生物化学
- 遗传学 是一个遗传学.
- 分子生物学分子生物学
背景情况:
- 氧化应激源于反应性氧物种 (ROS) 生产和抗氧化防御的不平衡.
- 遗传因素显著影响个人对氧化应激和相关疾病的易感性.
- 氧化应激与许多生理和病理过程有关.
研究的目的:
- 审查氧化应激和遗传学之间的复杂关系.
- 突出抗氧化酶和抗氧化途径中的遗传多态性对氧化应激易感性的影响.
- 讨论与氧化压力相关的遗传变异在疾病发展和进展中的作用.
主要方法:
- 文献综述侧重于抗氧化酶中的遗传多态性 (例如,超氧化脱氧化酶,谷氨过氧化酶,催化酶).
- 对NRF2-KEAP1信号轴及其在氧化应激中的遗传调节的分析.
- 检查遗传变异与神经退行性疾病,心血管疾病,癌症和代谢综合征等疾病之间的关联.
主要成果:
- 关键抗氧化酶和NRF2-KEAP1通路中的遗传多态性调节了对氧化应激的敏感性.
- 特定的遗传变异与各种复杂疾病的发展和进展有关.
- 了解这些遗传影响对于阐明疾病机制至关重要.
结论:
- 氧化应激和遗传学之间的相互作用对于理解疾病病因学至关重要.
- 识别与氧化应激相关的遗传生物标志物可以帮助早期诊断和风险评估.
- 针对氧化应激途径的个性化治疗策略可以根据个体遗传特征开发.
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