发病机制
川地34
甲状腺
疾病
病理
生物
医学
细胞生物学
内科学
干细胞
作者
Bin Yu,Yi Wang,Jun‐O Jin,Jin Liu,Yazhuo Huang,Yang Wang,Chenfang Zhu,Yinwei Li,Bin Li,Jing Sun,Dan Li,Sijie Fang,Huifang Zhou
标识
DOI:10.1210/clinem/dgae876
摘要
The IL-6/STAT3/miR-182-5p pathway led to activation of CD34+ OFs. MiR-182-5p promoted the proliferation, migration, fibrosis, and anti-apoptosis of CD34+ OFs via targeting Smad7. Our findings suggest that miR-182-5p may potentially serve as a therapeutic target for TED.
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