The Interplay between Ca 2+ Signaling Pathways and Neurodegeneration.

Autor: Ureshino RP; Department of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP 09961-400, Brazil., Erustes AG; Department of Pharmacology, Universidade Federal de São Paulo, São Paulo, SP 04044-020, Brazil., Bassani TB; Department of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP 09961-400, Brazil., Wachilewski P; Department of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP 09961-400, Brazil., Guarache GC; Department of Pharmacology, Universidade Federal de São Paulo, São Paulo, SP 04044-020, Brazil., Nascimento AC; Department of Pharmacology, Universidade Federal de São Paulo, São Paulo, SP 04044-020, Brazil., Costa AJ; Department of Pharmacology, Universidade Federal de São Paulo, São Paulo, SP 04044-020, Brazil., Smaili SS; Department of Pharmacology, Universidade Federal de São Paulo, São Paulo, SP 04044-020, Brazil., Pereira GJDS; Department of Pharmacology, Universidade Federal de São Paulo, São Paulo, SP 04044-020, Brazil.
Jazyk: angličtina
Zdroj: International journal of molecular sciences [Int J Mol Sci] 2019 Nov 28; Vol. 20 (23). Date of Electronic Publication: 2019 Nov 28.
DOI: 10.3390/ijms20236004
Abstrakt: Calcium (Ca 2+ ) homeostasis is essential for cell maintenance since this ion participates in many physiological processes. For example, the spatial and temporal organization of Ca 2+ signaling in the central nervous system is fundamental for neurotransmission, where local changes in cytosolic Ca 2+ 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, Ca 2+ homeostasis is altered, with increased cytoplasmic Ca 2+ concentrations leading to the activation of proteases, lipases, and nucleases. This review aimed to highlight the role of Ca 2+ signaling in neurodegenerative disease-related apoptosis, where the regulation of intracellular Ca 2+ 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 α-synuclein, β-amyloid peptide (Aβ), and huntingtin all adversely affect Ca 2+ homeostasis. Due to the mounting evidence for the relevance of Ca 2+ signaling in neuroprotection, we would focus on the expression and function of Ca 2+ signaling-related proteins, in terms of the effects on autophagy regulation and the onset and progression of neurodegenerative diseases.
Competing Interests: The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
Databáze: MEDLINE
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