发病机制
急性肾损伤
紧密连接
肾
肾脏疾病
医学
细胞生物学
癌症研究
生物
免疫学
内科学
作者
Wei Wei,Weiying Li,Luxi Yang,Savidya Weeramantry,Liang Ma,Ping Fu,Yuliang Zhao
摘要
Abstract Acute kidney injury (AKI) is characterized by a rapid reduction in kidney function caused by various etiologies. Tubular epithelial cell dysregulation plays a pivotal role in the pathogenesis of AKI. Tight junction (TJ) is the major molecular structure that connects adjacent epithelial cells and is critical in maintaining barrier function and determining the permeability of epithelia. TJ proteins are dysregulated in various types of AKI, and some reno‐protective drugs can reverse TJ changes caused by insult. An in‐depth understanding of TJ regulation and its causality with AKI will provide more insight to the disease pathogenesis and will shed light on the potential role of TJs to serve as novel therapeutic targets in AKI.
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