Calcium (Ca{}^{2+}) plays a critical role in podocyte function. The Ca{}^{2+}-sensitive receptors on the cell surface can sense changes in Ca{}^{2+} concentration, and Ca{}^{2+} flow into podocytes, after activation of Ca{}^{2+} channels (such as transient receptor potential canonical (TRPC) channels and N-type calcium channels) by different stimuli. In addition, the type 2 ryanodine receptor (RyR2) and the voltage-dependent anion channel 1 (VDAC1) on mitochondrial store-operated calcium channels (SOCs) on the endoplasmic reticulum maintain the Ca{}^{2+} homeostasis of the organelle. Ca{}^{2+} signaling is transmitted through multiple downstream signaling pathways and participates in the morphogenesis, structural maintenance, and survival of podocytes. When Ca{}^{2+} is dysregulated, it leads to the occurrence and progression of various diseases, such as focal segmental glomerulosclerosis, diabetic kidney disease, lupus nephritis, transplant glomerulopathy, and hypertensive renal injury. Ca{}^{2+} signaling is a promising therapeutic target for podocyte-related diseases. This review first summarizes the role of Ca{}^{2+} sensing, Ca{}^{2+} channels, and different Ca{}^{2+}-signaling pathways in the biological functions of podocytes, then, explores the status of Ca{}^{2+} signaling in different podocyte-related diseases and its advances as a therapeutic target.