肾脏疾病
急性肾损伤
医学
氧化应激
自噬
炎症
内科学
缺氧(环境)
病理
心脏病学
肾功能
细胞凋亡
生物
化学
有机化学
氧气
生物化学
作者
Liyu He,Qingqing Wei,Jing Liu,Mixuan Yi,Yu Liu,Hong Liu,Lin Sun,Youming Peng,Fuyou Liu,Manjeri A. Venkatachalam,Zheng Dong
标识
DOI:10.1016/j.kint.2017.06.030
摘要
Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected. Although AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in patients with CKD, is known to be more severe and difficult to recover. CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of transforming growth factor-β, p53, hypoxia-inducible factor, and major developmental pathways. At the cellular level, CKD is characterized by mitochondrial dysfunction, oxidative stress, and aberrant autophagy. At the tissue level, CKD is characterized by chronic inflammation and vascular dysfunction. These pathologic changes may contribute to the heightened sensitivity of, and nonrecovery from, AKI in patients with CKD.
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