A Putative Prohibitin-Calcium Nexus in -Cell Mitochondria and Diabetes.

The role of mitochondria in apoptosis is well known; however, the mechanisms linking mitochondria to the proapoptotic effects of proinflammatory cytokines, hyperglycemia, and glucolipotoxicity are not completely understood. Complex Ca signaling has emerged as a critical contributor to these proapoptotic effects and has gained significant attention in regulating the signaling processes of mitochondria. In pancreatic -cells, Ca plays an active role in -cell function and survival. Prohibitin (PHB), a mitochondrial chaperone, is actively involved in maintaining the architecture of mitochondria. However, its possible interaction with Ca-activated signaling pathways has not been explored. The present review aims to examine potential crosstalk between Ca signaling and PHB function in pancreatic -cells. Moreover, this review will focus on the effects of cytokines and glucolipotoxicity on Ca signaling and its possible interaction with PHB. Improved understanding of this important mitochondrial protein may aid in the design of more targeted drugs to identify specific pathways involved with stress-induced dysfunction in the -cell.