Calcium signaling as a mediator of cell energy demand and a trigger to cell death

• Published in: Annals of the New York Academy of Sciences Vol. 1350; no. 1; pp. 107 - 116
• Main Authors: Bhosale, Gauri, Sharpe, Jenny A., Sundier, Stephanie Y., Duchen, Michael R.
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01.09.2015; Wiley Subscription Services, Inc; John Wiley and Sons Inc
• Subjects: Animals; Apoptosis; Calcium; Calcium Signaling; Calcium-Binding Proteins - genetics; Calcium-Binding Proteins - metabolism; Cation Transport Proteins - genetics; Cation Transport Proteins - metabolism; Cell Death; Energy Metabolism; Humans; ischemia/reperfusion injury; MICU1; Mitochondria - metabolism; Mitochondria - pathology; mitochondrial calcium uptake; Mitochondrial Membrane Transport Proteins - genetics; Mitochondrial Membrane Transport Proteins - metabolism; Mitochondrial Membranes - chemistry; Mitochondrial Membranes - metabolism; Mitochondrial Membranes - pathology; mitochondrial permeability transition pore; Mitochondrial Proteins - genetics; Mitochondrial Proteins - metabolism; Models, Biological; Mutation; Necrosis; Original; Permeability; Phosphate Transport Proteins - genetics; Phosphate Transport Proteins - metabolism; Porosity; cell death; MICU1; ischemia/reperfusion injury; mitochondrial permeability transition pore; calcium signaling; mitochondrial calcium uptake
• ISSN: 0077-8923; 1749-6632
• DOI: 10.1111/nyas.12885

Calcium signaling is pivotal to a host of physiological pathways. A rise in calcium concentration almost invariably signals an increased cellular energy demand. Consistent with this, calcium signals mediate a number of pathways that together serve to balance energy supply and demand. In pathological states, calcium signals can precipitate mitochondrial injury and cell death, especially when coupled to energy depletion and oxidative or nitrosative stress. This review explores the mechanisms that couple cell signaling pathways to metabolic regulation or to cell death. The significance of these pathways is exemplified by pathological case studies, such as those showing loss of mitochondrial calcium uptake 1 in patients and ischemia/reperfusion injury.