足细胞
肾小球硬化
基因敲除
转录因子
细胞生物学
局灶节段性肾小球硬化
细胞外基质
调节器
肾
生物
抄写(语言学)
肾病
肾小球
功能(生物学)
信号转导
癌症研究
细胞外
化学
肾小球肾炎
肾功能
基因表达调控
肾脏疾病
基因表达
信使核糖核酸
发病机制
内科学
串扰
作者
Hiroko Hamatani,Akifumi Tabei,Shinichiro Ogawa,Junya Suwa,Rei Ishihara,Yuki Murakami,Toru Sakairi,Hidekazu Ikeuchi,Yoriaki Kaneko,H. Handa,Masato Morikawa,Akito Maeshima
出处
期刊:American Journal of Physiology-renal Physiology
[American Physical Society]
日期:2026-01-17
卷期号:330 (2): F269-F284
标识
DOI:10.1152/ajprenal.00336.2025
摘要
This study identifies atonal transcription factor 8 (ATOH8) as a previously unexplored regulator of podocyte function. We demonstrate that ATOH8 knockdown activates TGF-β signaling and increases extracellular matrix gene expression. Notably, ATOH8 deficiency alone does not cause renal injury but exacerbates glomerulosclerosis in an adriamycin-induced nephropathy model, accompanied by increased Tgfb1 mRNA expression in the renal cortex. These findings indicate that ATOH8 plays a protective role in podocyte function and limits glomerulosclerosis during kidney injury.
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