氧化应激:糖尿病病进展的一个罪祸首
1Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Antioxidants (Basel, Switzerland)
|April 27, 2024
概括
糖尿病病 (DKD) 源于与高血糖相关的氧化压力. 使用Nrf2激活剂和SGLT2抑制剂等药物向这种压力,有望减缓DKD的进展.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 内分泌学 在内分泌学.
- 生物化学 生物化学
背景情况:
- 糖尿病病 (DKD) 是慢性病 (CKD) 和末期病 (ESRD) 的主要原因.
- 对DKD病变的有限理解阻碍了有效的治疗.
- 由高血糖和活性氧物种 (ROS) 驱动的氧化应激是DKD发展和血管并发症的核心.
研究的目的:
- 审查目前关于针对DKD的有针对性的干预措施的临床前和临床发现.
- 评估氧化应激及其相关途径在DKD中的作用.
- 为了确定 DKD 治疗的有希望的治疗点.
主要方法:
- 临床前研究的全面评估.
- 对当前临床试验结果的分析.
- 专注于针对性干预,操纵关键分子通路.
主要成果:
- 过高血糖会增加ROS的产生,导致氧化应激并破坏氧化剂-抗氧化剂平衡.
- 激活的通路包括PI3K/Akt,TGF-β/p38-MAPK,NF-κB,AMPK,以及JAK/STAT. 这些通路都被激活.
- 临床试验显示,巴多克索隆甲基 (Nrf2激活剂),SGLT2抑制剂和GLP-1受体激动剂通过减少氧化应激来减缓DKD进展.
结论:
- 减少ROS是DKD的一个关键治疗策略.
- 巴多克索隆甲基,SGLT2抑制剂和GLP-1受体激动剂在减缓DKD方面是有效的.
- 抗氧化剂,Nox抑制剂,表观遗传调节剂和补充抑制剂提供了有前途的未来治疗选择.
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