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在慢性病中,SFN通过与MYH9结合促进纤维化

Fang Wang¹, Xiao-Guo Suo², Jia-Nan Wang²

¹Department of Pharmacy, Lu'an Hospital of Anhui Medical University, Lu'an People's Hospital of Anhui Province, Lu'an, 237006, China; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, The Key Laboratory of Anti-inflammatory of Immune Medicines, Ministry of Education, Hefei, 230032, China.

European journal of pharmacology

|July 10, 2024

概括

斯特拉提芬 (SFN) 通过与肌重链9 (MYH9) 相互作用,促进慢性病 (CKD) 中的纤维化. 减少SFN可能为治疗纤维化提供新的治疗策略.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
病理学病理学病理学

背景情况:

慢性病 (CKD) 标志着逐渐下降的功能和纤维化,缺乏有效的治疗方法.
纤维化是CKD的主要病理,需要新的治疗点.
斯特拉提芬 (SFN) 是一种涉及各种细胞功能的蛋白质.

研究的目的:

调查斯特拉提芬 (SFN) 在纤维化发展中的作用.
阐明SFN导致纤维化的分子机制.
探索SFN作为CKD治疗的潜在治疗点.

主要方法:

在CKD患者和模型中分析SFN表达.
在体外研究中,使用使用受TGF-β1.1.治疗的人类管上皮细胞进行了试验.
在体内研究使用单边尿路阻塞 (UUO) 鼠标模型.
分子测定包括LC-MS/MS,Co-IP和免疫光检测,以确定SFN相互作用伙伴.
对SFN和MYH9.9进行基因淘汰实验.

主要成果:

在CKD患者和纤维化模型中,SFN表达被上调.
转化生长因子β1 (TGF-β1) 诱导的纤维化被SFN敲击逆转.
在UUO小鼠中,SFN knockdown改善了管扩张和间歇性纤维化.
发现SFN在管状上皮细胞中与肌酸重链9 (MYH9) 结合.
Knockdown 的 MYH9 减少了纤维化标志物 (Col-1,α-SMA),和沉默 SFN 减少了 MYH9 表达,缓解纤维化.

结论:

斯特拉提芬 (SFN) 通过与MYH9.9的相互作用促进CKD中的纤维化.
SFN-MYH9相互作用代表了治疗纤维化的潜在治疗标.
向SFN-MYH9通路可能为慢性病提供新的治疗策略.

关键词:

慢性脏疾病慢性脏疾病在MYH9中,MYH9是MYH9的代号.患有脏纤维化在SFN中,SFN是最重要的.

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