Laboratory of Molecular and Cellular Signaling, Department of Molecular Cell Biology, K.U. Leuven, Campus Gasthuisberg O/N-1 bus 802, Herestraat 49, BE-3000 Leuven, Belgium.
Cell Calcium. 2011 Sep;50(3):242-50. doi: 10.1016/j.ceca.2011.04.001. Epub 2011 May 14.
Autophagy is a cellular process responsible for delivery of proteins or organelles to lysosomes. It participates not only in maintaining cellular homeostasis, but also in promoting survival during cellular stress situations. It is now well established that intracellular Ca(2+) is one of the regulators of autophagy. However, this control of autophagy by intracellular Ca(2+) signaling is the subject of two opposite views. On the one hand, the available evidence indicates that intracellular Ca(2+) signals, and mainly inositol 1,4,5-trisphosphate receptors (IP(3)Rs), suppress autophagy. On the other hand, elevated cytosolic Ca(2+) concentrations (Ca(2+)) were also shown to promote the autophagic process. Here, we will provide a critical overview of the literature and discuss both hypotheses. Moreover, we will suggest a model explaining how changes in intracellular Ca(2+) signaling can lead to opposite outcomes, depending on the cellular state.
自噬是一种负责将蛋白质或细胞器递送至溶酶体的细胞过程。它不仅参与维持细胞内稳态，而且在细胞应激情况下促进细胞存活。现在已经证实，细胞内 Ca(2+) 是自噬的调节剂之一。然而，细胞内 Ca(2+) 信号对自噬的这种控制是两种相反观点的主题。一方面，现有证据表明细胞内 Ca(2+) 信号，主要是肌醇 1,4,5-三磷酸受体 (IP(3)Rs)，抑制自噬。另一方面，也表明升高的胞质 Ca(2+) 浓度 (Ca(2+)) 促进自噬过程。在这里，我们将对文献进行批判性综述，并讨论这两种假说。此外，我们将提出一个模型，解释细胞内 Ca(2+) 信号的变化如何根据细胞状态导致相反的结果。
