ClC-3 chloride channel/antiporter defect contributes to inflammatory bowel disease in humans and mice

Conclusions
A defect in ClC-3 may contribute to the pathogenesis of IBD by promoting intestinal epithelial cell apoptosis and Paneth cell loss, suggesting that modulation of ClC-3 expression might be a new strategy for the treatment of IBD.

Source: Gut - September 2, 2014 Category: Gastroenterology Authors: Huang, L.-Y., He, Q., Liang, S.-J., Su, Y.-X., Xiong, L.-X., Wu, Q.-Q., Wu, Q.-Y., Tao, J., Wang, J.-P., Tang, Y.-B., Lv, X.-F., Liu, J., Guan, Y.-Y., Pang, R.-P., Zhou, J.-G. Tags: Crohn's disease Inflammatory bowel disease Source Type: research