Author(s): Cerella C, Diederich M, Ghibelli L
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Abstract Ca(2+) is an important second messenger participating in many cellular activities; when physicochemical insults deregulate its delicate homeostasis, it acts as an intrinsic stressor, producing/increasing cell damage. Damage elicits both repair and death responses; intriguingly, in those responses Ca(2+) also participates as second messenger. This delineates a dual role for Ca(2+) in cell stress, making difficult to separate the different and multiple mechanisms required for Ca(2+)-mediated control of cell survival and apoptosis. Here we attempt to disentangle the two scenarios, examining on the one side, the events implicated in deregulated Ca(2+) toxicity and the mechanisms through which this elicits reparative or death pathways; on the other, reviewing the role of Ca(2+) as a messenger in the transduction of these same signaling events.
This article was published in Int J Cell Biol
and referenced in Journal of Cancer Science & Therapy