在慢性非细菌性前列腺炎中,表皮氧还原应激通过ZNF24-MIF-NF-κB通路对巨细胞免疫代谢进行程序
Fei Zhang1, Andong Zhang1, Tong Meng1
1Department of Urology, The First Affiliated Hospital of Anhui Medical University, Institute of Urology, and Anhui Province Key Laboratory of Genitourinary Diseases, Anhui Medical University, 218 Jixi Road, Shushan District, Hefei, Anhui, 230022, People's Republic of China.
Redox biology
|January 23, 2026
概括
研究人员确定了一条关键的信号通路,涉及表皮氧还原应激和长期非细菌性前列腺炎 (CNP) 中的巨细胞激活. 针对这种途径,包括巨细胞迁移抑制因子 (MIF) 和PKM2,为这种耐火性疾病提供了潜在的新疗法.
科学领域:
- 免疫学 免疫学 免疫学
- 泌尿器科 泌尿器科 泌尿器科 泌尿器科
- 细胞生物学 细胞生物学
背景情况:
- 慢性非细菌性前列腺炎 (CNP) 是一种常见且难以治疗的疾病,免疫机制不明.
- 氧化还原失衡是慢性炎症的一个已知的因素.
研究的目的:
- 调查表皮氧氧化还原应激在 CNP 期间免疫调节中的作用.
- 阐明导致慢性前列腺炎症的分子机制.
主要方法:
- 综合性血细胞因子分析,批量和单细胞转录组学.
- 使用实验性自身免疫性前列腺炎 (EAP) 模型.
- 进行了体外和体内生物药理干预.
主要成果:
- 鉴定了作为一个关键的介导体的表皮衍生的巨细胞迁移抑制因子 (MIF).
- 发现反应性氧物种 (ROS) 激活ZNF24,促进MIF转录.
- MIF在巨细胞上接触CD74,稳定PKM2,增强糖解,并激活NF-κB,驱动M1极化和炎症.
- 针对MIF,CD74,PKM2或NF-κB减弱的炎症和盆腔疼痛.
结论:
- 在CNP中定义了一个新的上皮ROS-ZNF24-MIF-巨CD74-PKM2-NF-κB信号轴.
- 这一途径通过增强的糖解和炎症促进M1巨细胞的两极分化.
- 这条通路中的氧化敏感节点是 CNP 中精密免疫调节的有希望的目标.
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