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抑制PGRN可以缓解肺纤维化,调节Akt/GSK3β信号通路

Tian Xie¹, Yamei Zheng¹, Lei Zhang¹

¹Department of Pulmonary and Critical Care Medicine, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan, 570311, China.

International immunopharmacology

|March 15, 2025

概括

通过调节Akt/GSK3β通路,降低PGRN可以缓解肺纤维化 (PF). 这表明PGRN是治疗肺纤维化的潜在治疗标.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
病理学病理学病理学

背景情况:

肺纤维化 (PF) 是一种渐进的肺病,其特点是过度的原沉积和肺结构崩.
目前的治疗方法,如宁泰达尼布和皮尔费尼,具有有限的疗效和显著的副作用,突出了对新治疗策略的需求.
导致PF进展的分子机制尚不完全理解,需要对潜在的治疗点进行进一步的研究.

研究的目的:

为了研究 pregranuloprotein (PGRN) 在肺纤维化病变的分子机制.
在PF的体外和体外模型中评估向PGRN的治疗潜力.

主要方法:

建立了体外 (用TGF-β1治疗的MRC-5细胞) 和体内 (小鼠中的白素诱导的PF) 模型.
在患者血中测量了PGRN mRNA表达,并使用siRNAs评估了PGRN淘汰的影响.
通过各种生化和组织学技术分析了细胞增殖,细胞亡,炎症标记物,纤维化标记物和Akt/GSK3β信号通路.

主要成果:

在PF患者的血中观察到升高的PGRNmRNA表达.
试验室中PGRN淘汰减少了亲纤维细胞和炎症标志物,并抑制了Akt/GSK3β通路的激活.
在体内,PGRN敲击减轻了白血素诱导的PF小鼠模型中的肺炎,纤维化和气膜破坏,与Akt/GSK3β通路的调制相关.

结论:

抑制PGRN证明了在减轻肺纤维化中的治疗效果,无论是体外还是体内.
该机制涉及Akt/GSK3β信号通路的调制.
PGRN成为一个有前途的潜在治疗标或肺纤维化辅助疗法.

关键词:

布莱莫辛是一种白色素.在PGRNN中使用.肺部纤维化肺部纤维化信号通道的信号通道.在TGF-β1中.

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