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HIF-1介导的巨细胞代谢重编程促进了AKI到CKD的过渡

Hong Ding^1,2, Yan Zhou¹, Ren-He Zhu¹

¹Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, P.R. China.

International journal of biological sciences

|October 13, 2025

概括

亲炎性巨细胞在急性损伤 (AKI) 到慢性病 (CKD) 过渡期间驱动纤维化. 向巨细胞中的NF-κB-HIF-1信号通路为这种进展提供了潜在的治疗策略.

科学领域:

腎臟病學 (nephrology) 是一種醫學.
免疫学免疫学免疫学
代谢途径代谢途径

背景情况:

从急性损伤 (AKI) 过渡到慢性病 (CKD) 的特征是不适应性修复,其中巨细胞参与是关键特征.
巨细胞对这种不适应性修复和随后的纤维化有所贡献的精确机制仍然不完全理解.

研究的目的:

阐明亲炎性巨细胞在AKI过渡到CKD期间脏不适应性修复中的作用.
调查潜在的分子机制,包括代谢重编程和信号通路,调节巨细胞的功能在这种情况下.

主要方法:

宏细胞枯竭实验,以评估它们对管间纤维化病的贡献.
对巨细胞糖解的分析及其对HIF-1α的依赖.
在髓状细胞中研究NF-κB和HIF-1α之间的调控关系.
在体内研究使用骨髓细胞特异性HIF-1α淘汰模型和NF-κB抑制来评估治疗潜力.

主要成果:

巨细胞的枯竭显著减轻了管间纤维化和AKI到CKD的过渡.
葡萄糖分解被确定为维持促炎性巨细胞表型的必要条件.
骨髓状HIF-1α淘汰赛缓解了管间纤维化和AKI到CKD进展.
发现NF-κB直接与HIF-1α促进体结合,增强其转录并导致纤维化;NF-κB阻断改善了CKD的进展.

结论:

亲炎性巨细胞协调脏不适应性修复,驱动AKI向CKD过渡.
NF-κB-HIF-1信号轴调节巨细胞的代谢重编程,并促进纤维化.
针对这种信号通路是预防或治疗AKI后CKD进展的有希望的治疗策略.

关键词:

在 NF-κBB 中.急性脏损伤急性脏损伤是什么慢性脏疾病慢性脏疾病低氧诱导因子-1 诱导因子-1 巨细胞是一个巨细胞.代谢重编程是指代谢重编程.

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