ITPRs/inositol 1,4,5-trisphosphate receptors in autophagy: From enemy to ally.
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.
a KU Leuven Department of Microbiology and Immunology, Laboratory of Abdominal Transplantation; University Hospitals Leuven Department of Abdominal Transplant Surgery ; Leuven , Belgium.
Jean-Paul
JP
Decuypere
b KU Leuven Department of Cellular and Molecular Medicine, Laboratory of Molecular and Cellular Signaling ; Leuven , Belgium.
Jan B
JB
Parys
b KU Leuven Department of Cellular and Molecular Medicine, Laboratory of Molecular and Cellular Signaling ; Leuven , Belgium.
Geert
G
Bultynck
D000818:Animals; D001343:Autophagy / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology*; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism*; D053496:Inositol 1,4,5-Trisphosphate Receptors / Q000378:metabolism*
D053496:Inositol 1,4,5-Trisphosphate Receptors; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium
Ca2+ microdomains; Ca2+ signaling; autophagic flux; autophagy; inositol 1,4,5-trisphosphate receptor; spatio-temporal Ca2+ signals