利索酶通过JAK/STAT3信号通路促进纤维化在糖尿病病中
Yan Ren1, Mengjie Yu1, Danna Zheng1
1Nephrology Center, Department of Nephrology, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, China.
Archives of medical science : AMS
|February 28, 2024
概括
酶 (LYZ) 通过激活JAK/STAT3通路,促进糖尿病病中的纤维化. 葡萄糖可能通过增加LYZ分泌来增强纤维细胞增殖,从而导致功能衰竭.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 糖尿病病 (DN) 是导致衰竭的主要原因.
- 溶酶 (LYZ),一种天生的免疫成分,已与病有关.
- 这项研究探讨了LYZ表达和DN之间的关联.
研究的目的:
- 识别和验证与DN相关的枢纽基因.
- 为了研究LYZ在DN病变发生中的作用.
- 阐明LYZ诱导纤维化背后的分子机制.
主要方法:
- 生物信息学分析和小鼠模型的链毒素诱导的DN.
- 在体内,LYZ敲击和过度表达实验.
- 免疫组织化学,马森染色,CCK-8测定,西部斑块和JAK抑制剂治疗.
主要成果:
- 葡萄糖 (25 mM) 在纤维细胞中提高LYZ表达的调节,促进其增殖.
- LYZ激活了JAK/STAT3通路,该通路被AG490.0.部分抑制.
- 过度表达LYZ与衰老的管状上皮细胞 (RTEC) 在体内相关.
结论:
- 通过JAK/STAT3信号通路,LYZ促进DN中的纤维化.
- 葡萄糖可能通过LYZ自分泌驱动纤维细胞增殖.
- LYZ是DN进展的关键调解者.
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