The Physiopathologic Roles of Calcium Signaling in Podocytes

• Published in: Frontiers in bioscience (Landmark. Print) Vol. 28; no. 10; p. 240
• Main Authors: Tu, Yu-Chi, Shu, Hua-Pan, Sun, Lu-Lu, Liao, Qian-Qian, Feng, Li, Ren, Ming, Yao, Li-Jun
• Format: Journal Article
• Language: English
• Published: IMR Press 18-10-2023
• Subjects: calcium; calcium signaling; disease; podocyte; target
• ISSN: 2768-6701; 2768-6698
• DOI: 10.31083/j.fbl2810240

Calcium (Ca2+) plays a critical role in podocyte function. The Ca2+-sensitive receptors on the cell surface can sense changes in Ca2+ concentration, and Ca2+ flow into podocytes, after activation of Ca2+ 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 Ca2+ homeostasis of the organelle. Ca2+ signaling is transmitted through multiple downstream signaling pathways and participates in the morphogenesis, structural maintenance, and survival of podocytes. When Ca2+ 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. Ca2+ signaling is a promising therapeutic target for podocyte-related diseases. This review first summarizes the role of Ca2+ sensing, Ca2+ channels, and different Ca2+-signaling pathways in the biological functions of podocytes, then, explores the status of Ca2+ signaling in different podocyte-related diseases and its advances as a therapeutic target.