糖尿病脑病变的分子和生化机制
Igor Belenichev1, Olena Aliyeva2, Olena Popazova3
1Department of Pharmacology and Medical Formulation with Course of Normal Physiology, Zaporizhzhia State Medical and Pharmaceutical University, Zaporizhzhia, Ukraine.
Acta biochimica Polonica
|November 22, 2023
概括
糖尿病会增加神经系统疾病的风险,如中风和痴呆症. 本综述探讨了高血糖和细胞应激如何导致糖尿病脑病变,强调HSP70作为潜在的治疗点.
科学领域:
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
背景情况:
- 糖尿病是神经系统疾病的重要危险因素,包括缺血性中风,血管痴呆和神经退行.
- 高血糖是这些与糖尿病相关的神经并发症的发病的一个关键因素.
研究的目的:
- 审查糖尿病脑病变背后的分子机制.
- 检查氧化应激,硫化系统变化和糖尿病中线粒体/内皮细胞功能障碍的作用.
- 专注于糖尿病脑病变中热冲击蛋白70 (HSP70) 的神经保护功能.
主要方法:
- 对糖尿病脑病变现有数据的文献综述.
- 分析分子机制,包括氧化应激,硫酸硫酸盐平衡和细胞功能障碍.
- 研究HSP70作为细胞内伴侣和神经保护剂的作用.
主要成果:
- 过高血糖会触发糖尿病中神经系统疾病的发病.
- 氧化应激,二硫化物系统的改变以及线粒体/内皮功能障碍都与糖尿病脑病变有关.
- HSP70作为一种内源性神经保护剂,有助于蛋白质折叠,运输和降解.
结论:
- 在糖尿病脑病变中,HSP70对细胞反应至关重要.
- HSP70作为细胞内伴侣,在压力下维持蛋白质平衡.
- 作为一种分子标记物和治疗点,HSP70在治疗糖尿病及其神经复杂症方面表现有前途.
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