The Interplay between Ca2+ Signaling Pathways and Neurodegeneration

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]

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

• 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