Pizzo 2012 Pflugers Arch
Pizzo P, Drago I, Filadi R, Pozzan T (2012) Mitochondrial CaΒ²βΊ homeostasis: mechanism, role, and tissue specificities. Pflugers Arch 464:3β17. |
Pizzo P, Drago I, Filadi R, Pozzan T (2012) Pflugers Arch
Abstract: Mitochondria from every tissue are quite similar in their capability to accumulate CaΒ²βΊ in a process that depends on the electrical potential across the inner membrane; it is catalyzed by a gated channel (named mitochondrial CaΒ²βΊ uniporter), the molecular identity of which has only recently been unraveled. The release of accumulated CaΒ²βΊ in mitochondria from different tissues is, on the contrary, quite variable, both in terms of speed and mechanism: a NaβΊ-dependent efflux in excitable cells (catalyzed by NCLX) and a HβΊ/CaΒ²βΊ exchanger in other cells. The efficacy of mitochondrial CaΒ²βΊ uptake in living cells is strictly dependent on the topological arrangement of the organelles with respect to the source of CaΒ²βΊ flowing into the cytoplasm, i.e., plasma membrane or intracellular channels. In turn, the structural and functional relationships between mitochondria and other cellular membranes are dictated by the specific architecture of different cells. Mitochondria not only modulate the amplitude and the kinetics of local and bulk cytoplasmic CaΒ²βΊ changes but also depend on the CaΒ²βΊ signal for their own functionality, in particular for their capacity to produce ATP. In this review, we summarize the processes involved in mitochondrial CaΒ²βΊ handling and its integration in cell physiology, highlighting the main common characteristics as well as key differences, in different tissues. β’ Keywords: Mitochondria, Ca2+, MCU, NCLX β’ Bioblast editor: Cecatto C
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2020-02