Division of Nephrology and Kidney Research Institute, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Department of Internal Medicine, Florida Hospital/AdventHealth, Orlando, Florida, USA.
J Cell Physiol. 2023 Apr;238(4):727-741. doi: 10.1002/jcp.30976. Epub 2023 Feb 23.
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.
急性肾损伤 (AKI) 的特征是由各种病因引起的肾功能迅速下降。肾小管上皮细胞失调在 AKI 的发病机制中起关键作用。紧密连接 (TJ) 是连接相邻上皮细胞的主要分子结构，对于维持屏障功能和决定上皮通透性至关重要。在各种类型的 AKI 中，TJ 蛋白失调，一些肾保护药物可以逆转损伤引起的 TJ 变化。深入了解 TJ 的调节及其与 AKI 的因果关系将为疾病发病机制提供更多的认识，并阐明 TJ 作为 AKI 新型治疗靶点的潜在作用。
