Effect of TMEM16A on Renal Crystal Clearance and Tubule Dilation

Renal tubules maintain kidney homeostasis by clearing calcium oxalate (CaOx) microcrystals, yet the underlying cellular mechanisms remain unclear. TMEM16A, a Ca²⁺-activated chloride channel involved in ion transport and fluid secretion, may contribute to tubular dilation and crystal clearance. This study aims to determine whether TMEM16A is induced by CaOx crystal stress and whether its activity is required for tubular dilation and effective crystal removal. Using a mouse model of sodium oxalate–induced crystal formation, TMEM16A expression and localization will be assessed by western blotting and immunofluorescence, with histological analysis of crystal deposition and tubular morphology. Its functional role will be tested using selective inhibitors, with outcomes measured by crystal accumulation and tubular dilation. We hypothesize that TMEM16A is upregulated in response to crystal injury and promotes fluid secretion and structural changes for efficient crystal clearance.