TY - JOUR T1 - Modulation of Autophagy by Calcium Signalosome in Human Disease JF - Molecular Pharmacology JO - Mol Pharmacol DO - 10.1124/mol.116.105171 SP - mol.116.105171 AU - Eduardo Cremonese Filippi-Chiela AU - Michelle Stumpf Viegas AU - Marcos Thome AU - Andreia Buffon AU - Marcia R. Wink AU - Guido Lenz Y1 - 2016/01/01 UR - http://molpharm.aspetjournals.org/content/early/2016/07/19/mol.116.105171.abstract N2 - Autophagy is a catabolic process largely regulated by extra- and intracellular signaling pathways that are mainly involved in cellular metabolism and growth. However, mounting evidence has shown that ion channels and transporters are important for basal autophagy functioning and may also influence autophagy to deal with stressful situations. Besides its role in cell proliferation and apoptosis, intracellular Ca2+ is widely recognized as a key regulator of autophagy, acting through the modulation of pathways such as mTORC1, CaMKK2 and Protein Kinase C. Proper spatio-temporal Ca2+ availability coupled with a controlled ionic flow between storage compartments and the cytosol are critical to determine the effect of Ca2+ on autophagy and, consequently, on cell fate. Indeed, the crosstalk between Ca2+ and autophagy plays a central role in cellular homeostasis and survival during several physiological and pathological conditions. Here we review the main findings concerning the mechanisms and roles of Ca2+-modulated autophagy focusing in human disorders, from cancer to neurological diseases and infection. By identifying mechanisms and pathways that either induce or suppress autophagy, new promising approaches for preventing and treating related human disorders emerge, including some based on the modulation of Ca2+-mediated autophagy. ER -