Decuypere Jean-Paul, Parys Jan B, Bultynck Geert
a KU Leuven Department of Microbiology and Immunology, Laboratory of Abdominal Transplantation; University Hospitals Leuven Department of Abdominal Transplant Surgery ; Leuven , Belgium.
b KU Leuven Department of Cellular and Molecular Medicine, Laboratory of Molecular and Cellular Signaling ; Leuven , Belgium.
Autophagy. 2015;11(10):1944-8. doi: 10.1080/15548627.2015.1083666.
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.
肌醇三磷酸受体（ITPRs）是内质网（ER）主要的钙离子释放通道，最初被认为是自噬的抑制因子。然而，近年来积累的新证据支持ITPRs在驱动自噬通量方面发挥关键的刺激作用。在此，我们提供了一个综合观点，即ITPR介导的钙离子信号如何根据时空钙离子信号的特征，包括内质网-线粒体和内质网-溶酶体钙离子信号微区的存在，对自噬产生双重影响。
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