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Updated: Jan 20, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

通过PI3K-AKT介导的巨细胞激活,NMI作为急性胰腺炎的新型促炎驱动因素

Xiaoran Guo¹, Zhenting Liu¹, Zhuangfeng Weng²

¹Shenzhen Key Laboratory for Systems Medicine in Inflammatory Diseases, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.

|January 19, 2026

概括

N-myc和STAT交互因子 (NMI) 被确定为急性胰腺炎 (AP) 的关键媒介. 针对NMI及其下游途径可能为这种炎症性疾病提供新的治疗方法.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
胃肠病学胃肠病学

背景情况:

急性胰腺炎 (AP) 涉及全身炎症和多器官衰竭.
失调的先天免疫和与损伤相关的分子模式 (DAMPs) 是AP病变的核心.
在AP中放大系统性免疫激活的分子媒介在很大程度上是未知的.

研究的目的:

在AP中确定驱动持续免疫激活的分子媒介.
调查N-myc和STAT交互因子 (NMI) 在AP病变发生中的作用.
评估NMI作为AP的诊断生物标志物和治疗标.

主要方法:

在人类AP患者和小鼠模型中进行集成批量和单细胞转录组分析.
在胰腺组织,血液循环和远端器官中分析NMI表达.
使用重组NMI的体外研究和使用Nmi遗传切除和PI3K-AKT抑制的体内实验.

主要成果:

在AP中,NMI一直在上调,特别是在巨细胞和中性粒细胞中.
循环中的NMI水平准确地区分了AP患者与健康对照.
NMI激活巨细胞,促进IL-6和TNF分泌;IL-6被确定为一个关键的下游效应因子.
在体内,NMI抑制或PI3K-AKT通路阻塞减轻了AP严重程度和系统性炎症.

结论:

在AP中,NMI是关键的DAMP调解器和炎症驱动器.
NMI 作为 AP 的潜在诊断生物标志物.
针对NMI-PI3K-AKT途径为AP提供了一个有前途的治疗策略.

关键词:

这就是为什么APAPAPAPAP.与损伤相关的分子模式巨细胞激活活动在NMI中,NMI是NMI.在PI3K-AKT信号传输中.

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