慢性病中的压力途径:将皮质醇,氧化压力和炎症联系起来
Maria Motrenikova1, Krasimir Boyanov1, Neli Bojinova2
1Department of Medical Biochemistry, Faculty of Pharmacy, Medical University of Plovdiv, Vasil Aprilov Str. 15A, 4002 Plovdiv, Bulgaria.
Antioxidants (Basel, Switzerland)
|October 29, 2025
概括
慢性压力和下丘脑-垂体-上腺 (HPA) 轴功能障碍通过破坏精神神经内分泌-免疫系统来加速慢性病 (CKD). 针对氧化应激,炎症和HPA轴不平衡可能会改善CKD的结果.
科学领域:
- 内分泌学和脏学.
- 心理神经免疫学 心理神经免疫学
- 分子医学是分子医学.
背景情况:
- 慢性病 (CKD) 涉及氧化应激,炎症和神经内分泌失衡.
- 心理神经内分泌免疫系统 (PNEI) 在CKD病变发生过程中起着至关重要的作用.
- 下丘脑-垂体-上腺 (HPA) 轴的调节失调与CKD有关.
研究的目的:
- 审查将慢性压力和HPA轴失调与CKD联系在一起的证据.
- 探索皮质醇,氧化应激,炎症和CKD中的代谢因素的相互作用.
- 突出 PNEI 系统在 CKD 进展中的作用.
主要方法:
- 文献综述综合实验和临床发现.
- 对与氧化应激 (MDA,AOPPs,8-OHdG),炎症 (TNF-α,IL-1β,IL-6) 和皮质醇动态相关的生物标志物的分析.
- 在CKD中整合PNEI系统组件的数据.
主要成果:
- 亲炎性调解剂和氧化应激标志物与CKD进展有关.
- 改变的皮质醇模式表明慢性HPA激活,导致免疫和代谢功能障碍.
- 压力诱导的PNEI系统失调会放大损伤和全身并发症.
结论:
- PNEI系统的相互连接机制极大地影响了CKD的进展.
- 氧化,炎症和神经内分泌生物标志物的联合评估可能会增强CKD风险分层.
- 针对PNEI系统失调,为CKD提供了潜在的治疗策略.
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