Calcium Signaling in Human Health and Diseases

Dear Colleagues,

Intracellular Ca²⁺ signals regulate a myriad of cellular functions, ranging from short-term responses, such as excitation–contraction coupling and stimulus–secretion coupling, to long-term processes, such as proliferation, gene expression, differentiation, motility, synaptic plasticity, programmed cell death (or apoptosis) and metabolism. It is, therefore, not surprising that any derangement of the multifaceted Ca²⁺ toolkit that shapes the elevation in intracellular Ca²⁺ concentration ([Ca²⁺]_i) may lead to severe pathological disorders, including cancer, neurodegenerative diseases, heart failure, severe combined immunodeficiency (SCID), deafness, pancreatitis, hypertension, and so on. An increase in [Ca²⁺]_i is shaped by the concerted interaction among the components of an extremely versatile network of channels, transporters, pumps and buffer that can be uniquely assembled by each cell type to generate intracellular Ca²⁺ signals with spatio-temporal properties precisely tailored to regulate specific functions. We are witnessing a fascinating period of ground-breaking discoveries in the Ca²⁺ signalling field, as testified by the identification of the first structural molecular components of the mitochondrial Ca²⁺ uniporter and permeability transition pore, by the discovery of many unexpected regulators of intracellular Ca²⁺ dynamics, such as p53, PML, and PTEN, and by the evidence that a growing number of pathologies is associated to mutations in Ca²⁺-permeable channels and/or Ca²⁺-regulated pathways. I am, therefore, pleased to invite all of you to participate to this Special Issue, "Calcium Signaling in Human Health and Diseases", by presenting your most recent research or ideas about the pathophysiological role of Ca²⁺. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Dr. Francesco Moccia
Guest Editor

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