肺动脉高压
发病机制
下调和上调
肺动脉
医学
机制(生物学)
细胞内
血管平滑肌
反馈回路
反馈调节
体外
心脏病学
内科学
泛素
非正面反馈
疾病
调节器
缺氧(环境)
血管疾病
血管阻力
血管壁
正面反馈
平滑肌
反馈控制
心肌细胞
循环(图论)
肺病
基因表达调控
肺血管系统
细胞生物学
药理学
病理生理学
生物信息学
遗传增强
信号转导
内皮功能障碍
作者
Mingzhou Guo,Ke Li,Yuchen Huang,Xuezhao Wang,Yuanzhou He,Congyi Wang,Jin Zhao,Xiansheng Liu,Li X
出处
期刊:Hypertension
[Lippincott Williams & Wilkins]
日期:2026-05-08
标识
DOI:10.1161/hypertensionaha.125.25501
摘要
BACKGROUND: Hypoxic pulmonary hypertension (HPH) is a representative vascular remodeling disease with a poor prognosis. Previous findings from our study have implicated the NICD4 (NOTCH4 intracellular domain) in pulmonary artery smooth muscle cells (PASMCs) in the pathogenesis of HPH. However, the underlying regulatory mechanisms remain unclear. In this study, we aimed to elucidate the potential regulatory mechanism of NICD4 in HPH. METHODS: ) mice and in vitro using primarily cultured PASMCs, alongside pharmacological inhibition with DUB-IN-2. RESULTS: can be transcriptionally upregulated by CSL/NICD4 under hypoxia, forming a NICD4/USP8-positive feedback loop. CONCLUSIONS: Our study unveils a critical NICD4/USP8-positive feedback loop that drives HPH pathogenesis, highlighting the importance of ubiquitination in pulmonary vascular remodeling. Targeted disruption of this loop represents a promising therapeutic strategy for HPH.
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