Abstract
Mitochondria play key roles in ATP supply, calcium homeostasis, redox balance control and apoptosis, which in neurons are fundamental for neurotransmission and to allow synaptic plasticity. Their functional integrity is maintained by mitostasis, a process that involves mitochondrial transport, anchoring, fusion and fission processes regulated by different signaling pathways but mainly by the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). PGC-1α also favors Ca2+ homeostasis, reduces oxidative stress, modulates inflammatory processes and mobilizes mitochondria to where they are needed. To achieve their functions, mitochondria are tightly connected to the endoplasmic reticulum (ER) through specialized structures of the ER termed mitochondria-associated membranes (MAMs), which facilitate the communication between these two organelles mainly to aim Ca2+ buffering. Alterations in mitochondrial activity enhance reactive oxygen species (ROS) production, disturbing the physiological metabolism and causing cell damage. Furthermore, cytosolic Ca2+ overload results in an increase in mitochondrial Ca2+, resulting in mitochondrial dysfunction and the induction of mitochondrial permeability transition pore (mPTP) opening, leading to mitochondrial swelling and cell death through apoptosis as demonstrated in several neuropathologies. In summary, mitochondrial homeostasis is critical to maintain neuronal function; in fact, their regulation aims to improve neuronal viability and to protect against aging and neurodegenerative diseases.
Highlights
Mitochondria play key roles in Adenosine triphosphate (ATP) supply, calcium homeostasis, redox balance control and apoptosis, which in neurons are fundamental for neurotransmission and to allow synaptic plasticity
Mitochondria participateactively in calcium (Ca2+ ) homeostasis, a process reviewed in the present work, and this mitochondrial function is fundamental for neuronal activity [5].To achieve this aim, they are physically and functionally linked to the endoplasmic reticulum (ER) by specialized structures, mitochondria-associated membranes (MAMs), which have been proposed to be highly relevant in calcium buffering
These findings suggest that the activation of Wnt pathways prevents mitochondrial permeability transition pore (mPTP) opening and the mechanisms implied in this activity involve the inhibition of mitochondrial glycogen synthase synthase kinase kinase 3β (GSK3β) and/or the modulation of mitochondrial hexokinase II (HKII)
Summary
Of the total oxygen supply and up to 20% of total glucose intake [1], especially in the neuropil [2]. Mitochondria participateactively in calcium (Ca2+ ) homeostasis, a process reviewed in the present work, and this mitochondrial function is fundamental for neuronal activity [5].To achieve this aim, they are physically and functionally linked to the endoplasmic reticulum (ER) by specialized structures, mitochondria-associated membranes (MAMs), which have been proposed to be highly relevant in calcium buffering They are sites of juxtaposed ER and outer mitochondrial membrane (OMM), which facilitate organelle communication, allowing the regulation of Ca2+ fluxes from ER to mitochondria, among other cellular functions such aslipid synthesis and transport, and glucose metabolism [6]. We present a review of the role of the factors implicated in mitostasis and its relationship with Ca2+ and free radicals in health, aging and neurodegenerative processes
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