Calcium and cell death signaling in neurodegeneration and aging

Anais da Academia Brasileira de Ciências

Soraya Smaili¹  Hanako Hirata¹  Rodrigo Ureshino¹  Priscila T. Monteforte¹  Ana P. Morales¹  Mari L. Muler¹  Juliana Terashima¹  Karen Oseki¹  Tatiana R. Rosenstock¹  Guiomar S. Lopes¹  Claudia Bincoletto¹ 

[1],Universidade Federal de São Paulo Escola Paulista de Medicina Departamento de FarmacologiaSão Paulo SP ,Brasil

关键词: calcium;    apoptosis;    Bax;    mitochondria;    endoplasmic reticulum;    neurodegeneration and aging;    cálcio;    apoptose;    Bax;    mitocôndrias;    retículo endoplasmático;    neurodegeneração e envelhecimento;   

DOI  :  10.1590/S0001-37652009000300011

来源: SciELO

【 摘 要 】

Transient increase in cytosolic (Cac2+) and mitochondrial Ca2+ (Ca m2+) are essential elements in the control of many physiological processes. However, sustained increases in Ca c2+ and Ca m2+ may contribute to oxidative stress and cell death. Several events are related to the increase in Ca m2+, 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.

【 授权许可】

CC BY   
 All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License