Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Cell Biology, autophagic flux, autophagy, Ca2+ microdomains, Ca2+ signaling, inositol 1,4,5-trisphosphate receptor, spatio-temporal Ca2+ signals, ENDOPLASMIC-RETICULUM, BAX INHIBITOR-1, REGULATES AUTOPHAGY, LYSOSOMAL FUSION, CA2+ SIGNALS, CALCIUM, CHANNEL, BIOENERGETICS, INS(1,4,5)P-3, HOMEOSTASIS, Animals, Autophagy, Calcium, Calcium Signaling, Endoplasmic Reticulum, Humans, Inositol 1,4,5-Trisphosphate, Inositol 1,4,5-Trisphosphate Receptors, 0601 Biochemistry and Cell Biology, Biochemistry & Molecular Biology, 3101 Biochemistry and cell biology

Abstract:

ITPRs (inositol 1,4,5-trisphosphate receptors), the main endoplasmic reticulum (ER) Ca(2+)-release channels, were originally proposed as suppressors of autophagy. Yet, new evidence has accumulated over recent years supporting a crucial, stimulatory role for ITPRs in driving the autophagic flux. Here, we provide an integrated view on how ITPR-mediated Ca(2+) signaling can have a dual impact on autophagy, depending on the characteristics of the spatio-temporal Ca(2+) signals, including the existence of ER-mitochondrial and ER-lysosomal Ca(2+) signaling microdomains.