Cerella Claudia, Diederich Marc, Ghibelli Lina
Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg, 9 rue Edward Steichen, Luxembourg L-2540, Luxembourg.
Int J Cell Biol. 2010;2010:546163. doi: 10.1155/2010/546163. Epub 2010 Mar 15.
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.
钙离子(Ca²⁺)是参与多种细胞活动的重要第二信使;当物理化学损伤破坏其微妙的内稳态时,它作为一种内在应激源,导致/加剧细胞损伤。损伤引发修复和死亡反应;有趣的是,在这些反应中Ca²⁺也作为第二信使参与其中。这描绘了Ca²⁺在细胞应激中的双重作用,使得难以区分Ca²⁺介导的细胞存活和凋亡控制所需的不同且多样的机制。在这里,我们试图厘清这两种情况,一方面研究与失调的Ca²⁺毒性相关的事件以及其引发修复或死亡途径的机制;另一方面,回顾Ca²⁺作为信使在这些相同信号事件转导中的作用。