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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

The Interplay between Ca2+ Signaling Pathways and Neurodegeneration

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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
[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
Web of Science Citations: 0

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 type: 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 type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 13/20073-2 - Autophagy as a protective mechanism in senescent rats
Grantee:Soraya Soubhi Smaili
Support type: 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 type: Regular Research Grants