| Author(s): |
Ureshino, Rodrigo Portes
[1]
;
Erustes, Adolfo Garcia
[2]
;
Bassani, Taysa Bervian
[1]
;
Wachilewski, Patricia
[1]
;
Guarache, Gabriel Cicolin
[2]
;
Nascimento, Ana Carolina
[2]
;
Costa, Angelica Jardim
[2]
;
Smaili, Soraya Soubhi
[2]
;
da Silva Pereira, Gustavo Jose
[2]
Total Authors: 9
|
Calcium (Ca2+) homeostasis is essential for cell maintenance since this ion participates in many physiological processes. For example, the spatial and temporal organization of Ca2+ signaling in the central nervous system is fundamental for neurotransmission, where local changes in cytosolic Ca2+ concentration are needed to transmit information from neuron to neuron, between neurons and glia, and even regulating local blood flow according to the required activity. However, under pathological conditions, Ca2+ homeostasis is altered, with increased cytoplasmic Ca2+ concentrations leading to the activation of proteases, lipases, and nucleases. This review aimed to highlight the role of Ca2+ signaling in neurodegenerative disease-related apoptosis, where the regulation of intracellular Ca2+ homeostasis depends on coordinated interactions between the endoplasmic reticulum, mitochondria, and lysosomes, as well as specific transport mechanisms. In neurodegenerative diseases, alterations-increased oxidative stress, energy metabolism alterations, and protein aggregation have been identified. The aggregation of alpha-synuclein, beta-amyloid peptide (A beta), and huntingtin all adversely affect Ca2+ homeostasis. Due to the mounting evidence for the relevance of Ca2+ signaling in neuroprotection, we would focus on the expression and function of Ca2+ signaling-related proteins, in terms of the effects on autophagy regulation and the onset and progression of neurodegenerative diseases. (AU) |