Polycystins and cellular Ca2+ signaling

The cystic phenotype in autosomal dominant polycystic kidney disease is characterized by a profound dysfunction of many cellular signaling patterns, ultimately leading to an increase in both cell proliferation and apoptotic cell death. Disturbance of normal cellular Ca2+ signaling seems to be a primary event and is clearly involved in many pathways that may lead to both types of cellular responses. In this review, we summarize the current knowledge about the molecular and functional interactions between polycystins and multiple components of the cellular Ca2+-signaling machinery. In addition, we discuss the relevant downstream responses of the changed Ca2+ signaling that ultimately lead to increased proliferation and increased apoptosis as observed in many cystic cell types.