Nicotera P, Orrenius S
Department of Molecular Toxicology, Faculty of Biology, University of Konstanz, Germany.
Cell Calcium. 1998 Feb-Mar;23(2-3):173-80. doi: 10.1016/s0143-4160(98)90116-6.
One general signalling mechanism used to transfer the information delivered by agonists into appropriate intracellular compartments involves the rapid redistribution of ionised calcium throughout the cell, which results in transient elevations of the cytosolic free Ca2+ concentration. Various physiological stimuli increase [Ca2+]i transiently and, thereby, induce cellular responses. However, under pathological conditions, changes of [Ca2+]i are generally more pronounced and sustained. Marked elevations of [Ca2+]i activate hydrolytic enzymes, lead to exaggerated energy expenditure, impair energy production, initiate cytoskeletal degradation, and ultimately result in cell death. Such Ca(2+)-induced cytotoxicity may play a major role in several diseases, including neuropathological conditions such as chronic neurodegenerative diseases and acute neuronal losses (e.g. in stroke).
一种用于将激动剂传递的信息转移到适当细胞内区室的一般信号传导机制,涉及离子钙在整个细胞中的快速重新分布,这导致细胞质游离Ca2+浓度的短暂升高。各种生理刺激会使[Ca2+]i短暂升高,从而诱导细胞反应。然而,在病理条件下,[Ca2+]i的变化通常更明显且持续时间更长。[Ca2+]i的显著升高会激活水解酶,导致能量消耗过度,损害能量产生,引发细胞骨架降解,并最终导致细胞死亡。这种钙诱导的细胞毒性可能在几种疾病中起主要作用,包括神经病理状况,如慢性神经退行性疾病和急性神经元损失(如中风时)。