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Anais da Academia Brasileira de Ciências

versão impressa ISSN 0001-3765versão On-line ISSN 1678-2690

Resumo

SMAILI, Soraya et al. Calcium and cell death signaling in neurodegeneration and aging. An. Acad. Bras. Ciênc. [online]. 2009, vol.81, n.3, pp.467-475. ISSN 0001-3765.  http://dx.doi.org/10.1590/S0001-37652009000300011.

Transient increase in cytosolic (Cac2+) and mitochondrial Ca2+ (Cam2+) are essential elements in the control of many physiological processes. However, sustained increases in Cac2+ and Cam2+ may contribute to oxidative stress and cell death. Several events are related to the increase in Cam2+, including regulation and activation of a number of Ca2+ dependent enzymes, such as phospholipases, proteases and nucleases. Mitochondria and endoplasmic reticulum (ER) play pivotal roles in the maintenance of intracellular Ca2+ homeostasis and regulation of cell death. Several lines of evidence have shown that, in the presence of some apoptotic stimuli, the activation of mitochondrial processes maylead to the release of cytochrome c followed by the activation of caspases, nuclear fragmentation and apoptotic cell death. The aim of this review was to show how changes in calcium signaling can be related to the apoptotic cell death induction. Calcium homeostasis was also shown to be an important mechanism involved in neurodegenerative and aging processes.

Palavras-chave : calcium; apoptosis; Bax; mitochondria; endoplasmic reticulum; neurodegeneration and aging.

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