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Ca2+ signaling critically regulates a number of cellular functions and physiological processes. In vertebrates, extracellular Ca2+ concentration is about four orders of magnitude higher than in the cytosol, while some cellular compartments (e.g. sarco-endoplasmic reticulum and mitochondria) show higher Ca2+ concentration and function as intracellular stores. Several channels and transporters are responsible for Ca2+ compartmentalization; these structures are differentially expressed and regulated in different cell types and may therefore represent specific therapeutic targets in various diseases.
In this respect, blockers of voltage-dependent L-type Ca2+ channels (Cav1.2) have been successfully used for decades to treat hypertension, cardiac ischemia and supraventricular tachyarrhythmias, while blockers of T-channels (Cav3.2 ) and N-channels (Cav2.2) are used to treat epilepsy and pain. Ca2+ signaling also plays an important role in cancer, in processes such as cell proliferation and migration. Therefore, Ca2+ channels and transporters are potential therapeutic targets also in oncology. For many years Ca2+ has also been studied as the master regulator of neuronal transmission, being essential for neurotransmitter release; however, when cytosolic Ca2+ massively increases in neurons, for example following prolonged excitatory neurotransmission, such as those occurring in seizures, ischemia or trauma, it activates noxious pathways (excitotoxicity) which may lead to cell death.
In honoring the major scientific contribution of former Frontiers in Pharmacology Field Chief Editor Professor Theophile Godfraind to the understanding of the pharmacology of calcium channels and transporters, this Research Topic concerns the preclinical and clinical pharmacology of investigational compounds as well as the study of endogenous molecules, that, by targeting Ca+ channels and transporters, represent emerging therapeutic tools for diverse diseases.
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