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...

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Detalles Bibliográficos
Autores principales: Decuypere, Jean-Paul, Parys, Jan B, Bultynck, Geert
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2015
Materias:
Views and Commentaries
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4824608/
https://www.ncbi.nlm.nih.gov/pubmed/26291777
http://dx.doi.org/10.1080/15548627.2015.1083666
Descripción
Sumario: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.

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