Tight junction and kidney stone disease
Issued Date
2023-01-01
Resource Type
ISSN
21688362
eISSN
21688370
Scopus ID
2-s2.0-85158938693
Journal Title
Tissue Barriers
Rights Holder(s)
SCOPUS
Bibliographic Citation
Tissue Barriers (2023)
Suggested Citation
Rungrasameviriya P., Santilinon A., Atichartsintop P., Hadpech S., Thongboonkerd V. Tight junction and kidney stone disease. Tissue Barriers (2023). doi:10.1080/21688370.2023.2210051 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/82752
Title
Tight junction and kidney stone disease
Author's Affiliation
Other Contributor(s)
Abstract
Defects of tight junction (TJ) are involved in many diseases related to epithelial cell functions, including kidney stone disease (KSD), which is a common disease affecting humans for over a thousand years. This review provides brief overviews of KSD and TJ, and summarizes the knowledge on crystal-induced defects of TJ in renal tubular epithelial cells (RTECs) in KSD. Calcium oxalate (CaOx) crystals, particularly COM, disrupt TJ via p38 MAPK and ROS/Akt/p38 MAPK signaling pathways, filamentous actin (F-actin) reorganization and α-tubulin relocalization. Stabilizing p38 MAPK signaling, reactive oxygen species (ROS) production, F-actin and α-tubulin by using SB239063, N-acetyl-L-cysteine (NAC), phalloidin and docetaxel, respectively, successfully prevent the COM-induced TJ disruption and malfunction. Additionally, genetic disorders of renal TJ, including mutations and single nucleotide polymorphisms (SNPs) of CLDN2, CLDN10b, CLDN14, CLDN16 and CLDN19, also affect KSD. Finally, the role of TJ as a potential target for KSD therapeutics and prevention is also discussed.