Transport, cilia, and PKD: must we in (cyst) on interrelationships? Focus on 'Increased Na~+/H~+ exchanger activity on the apical surface of a cilium-deflcient cortical collecting duct principal cell model of poly cystic kidney disease'

摘要

identification of the genes involved in polycystic kidney disease (PKD) suggests that defects in ciliary function are a common feature (4). In renal tubular epithelia, primary cilia on the apical surface normally protrude into the tubular lumen where they can detect fluid flow, likely due to the bending of the cilium and the triggering of calcium transients. How the lack of a central cilium and the disruption of this sensing and signaling could lead to the development of a pathologic cystic phenotype remain a very active area of investigation.