纤维化
血管生成
氧化应激
肾缺血
线粒体分裂
肾
炎症
急性肾损伤
肾脏疾病
线粒体
线粒体ROS
基因敲除
生物
医学
癌症研究
内分泌学
再灌注损伤
内科学
缺血
细胞凋亡
细胞生物学
生物化学
作者
Chi-Ting Su,Daniel H. W. See,Yue-Jhu Huang,Tzu‐Ming Jao,Shin‐Yun Liu,Chih-Yi Chou,Chun‐Fu Lai,Wei‐Chou Lin,Chih‐Yuan Wang,Jenq‐Wen Huang,Kuan‐Yu Hung
标识
DOI：10.1161/circresaha.123.322494
摘要
Our study is the first to demonstrate that LTBP4 deficiency increases AKI severity, consequently leading to chronic kidney disease. Potential therapies focusing on LTBP4-associated angiogenesis and LTBP4-regulated DRP1-dependent mitochondrial division are relevant to renal injury.
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(2025-6-4)
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