Authors: Harumi Fujita, Yoko Hamazaki, Yumi Noda, Masanobu Oshima, Nagahiro Minato
DOI: 10.1371/journal.pone.0052272
Abstract Summary
Claudin-4 knockout mice develop fatal hydronephrosis due to urinary tract obstruction caused by urothelial hyperplasia. While tight junctions remain structurally intact with compensatory claudin-3 upregulation, mice show increased calcium and chloride excretion, suggesting claudin-4’s role in ion reabsorption. The findings reveal claudin-4 is essential for maintaining normal urothelial homeostasis.
Why Brain? 🧠
Claudin-4 protein deficiency causes fatal kidney swelling by triggering abnormal bladder lining growth that blocks urine flow, revealing its critical role in urinary tract health and function.
License: CC BY.
The image is AI-generated for illustrative purposes only. Courtesy of Midjourney.
