Apoptosis and Autophagy: Decoding Calcium Signals that Mediate Life or Death
- 1Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106
- 2Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio 44106
- 3Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio 44106
- 4Molecular Pharmacology and Chemistry Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021
- Correspondence: cwd{at}case.edu
Abstract
Calcium is a versatile and dynamic 2nd messenger that is essential for the survival of all higher organisms. In cells that undergo activation or excitation, calcium is released from the endoplasmic/sarcoplasmic reticulum to activate calcium-dependent kinases and phosphatases, thereby regulating numerous cellular processes; for example, apoptosis and autophagy. In the case of apoptosis, endogenous ligands or pharmacological agents induce prolonged cytosolic calcium elevation, which in turn leads to cell death. In contrast, there is now evidence that calcium regulates autophagy by several mechanisms, and these may be important for maintaining cell survival. Here we summarize what is known about how calcium regulates these life and death decisions. We pay particular attention to pathways that have been described in lymphocytes and cardiomyocytes, as these systems provide optimal models for understanding calcium signaling in the context of normal cell physiology.
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