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Calcium is utilised by cells in signalling and in regulating ATP production; it also contributes to cell survival and, when concentrations are unbalanced, triggers pathways for cell death. Mitochondria contribute to calcium buffering, meaning that mitochondrial calcium uptake and release is intimately related to cytosolic calcium concentrations. This review focuses on the proteins contributing to mitochondrial calcium homoeostasis, the roles of the mitochondrial permeability transition pore (MPTP) and mitochondrial calcium-activated proteins, and their relevance in neurodegenerative pathologies. It also covers alterations to calcium homoeostasis in Friedreich ataxia (FA).

More information Original publication

DOI

10.1042/NS20180061

Type

Journal article

Publication Date

2018-12-01T00:00:00+00:00

Volume

2

Keywords

calcium homoeostasis, mitochondria, mitochondrial permeability transition pore, neurodegeneration