Calcium Signaling Mediates Cell Death and Crosstalk with Autophagy in Kidney Disease

The kidney is an important organ for the maintenance of Ca(2+) homeostasis in the body. However, disruption of Ca(2+) homeostasis will cause a series of kidney diseases, such as acute kidney injury (AKI), chronic kidney disease (CKD), renal ischemia/reperfusion (I/R) injury, autosomal dominant polycystic kidney disease (ADPKD), podocytopathy, and diabetic nephropathy. During the progression of kidney disease, Ca(2+) signaling plays key roles in various cell activities such as necrosis, apoptosis, eryptosis and autophagy. Importantly, there are complex Ca(2+) flux networks between the endoplasmic reticulum (ER), mitochondria and lysosomes which regulate intracellular Ca(2+) signaling in renal cells and contribute to kidney disease. In addition, Ca(2+) signaling also links the crosstalk between various cell deaths and autophagy under the stress of heavy metals or high glucose. In this regard, we present a review of Ca(2+) signaling in cell death and crosstalk with autophagy and its potential as a therapeutic target for the development of new and efficient drugs against kidney diseases.