| Full text | |
| 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
|
| Affiliation: | [1] Univ Fed Sao Paulo, Dept Biol Sci, BR-09961400 Diadema, SP - Brazil
[2] Univ Fed Sao Paulo, Dept Pharmacol, BR-04044020 Sao Paulo, SP - Brazil
Total Affiliations: 2
|
| Document type: | Review article |
| Source: | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES; v. 20, n. 23 DEC 2019. |
| Web of Science Citations: | 0 |
| Abstract | |
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) | |
| FAPESP's process: | 16/20796-2 - Study of estrogen receptors mediated autophagy against tau toxicity in cell and zebrafish models |
| Grantee: | Rodrigo Portes Ureshino |
| Support Opportunities: | Research Grants - Young Investigators Grants |
| FAPESP's process: | 17/23616-8 - Analysis of progestagen receptors-mediated autophagy against tau toxicity in cell model of tauopathy |
| Grantee: | Taysa Bervian Bassani |
| Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
| FAPESP's process: | 13/20073-2 - Autophagy as a protective mechanism in senescent rats |
| Grantee: | Soraya Soubhi Smaili |
| Support Opportunities: | Regular Research Grants |
| FAPESP's process: | 17/10863-7 - Study of lipophagy mediated by two-pore channels receptors |
| Grantee: | Gustavo José da Silva Pereira |
| Support Opportunities: | Regular Research Grants |