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Mitostasis, calcium and free radicals in health, aging and neurodegeneration

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dc.contributor.author Godoy Zeballos, Juan Alejandro, 1959-
dc.contributor.author Rios, Juvenal A.
dc.contributor.author Picón-Pagès, Pol
dc.contributor.author Herrera-Fernández, Víctor
dc.contributor.author Swaby, Bronte
dc.contributor.author Crepin, Giulia
dc.contributor.author Vicente García, Rubén, 1978-
dc.contributor.author Fernández-Fernández, José Manuel, 1967-
dc.contributor.author Muñoz López, Francisco José, 1964-
dc.date.accessioned 2021-08-25T06:55:41Z
dc.date.available 2021-08-25T06:55:41Z
dc.date.issued 2021
dc.identifier.citation Godoy JA, Rios JA, Picón-Pagès P, Herrera-Fernández V, Swaby B, Crepin G, Vicente R, Fernández-Fernández JM, Muñoz FJ. Mitostasis, calcium and free radicals in health, aging and neurodegeneration. Biomolecules. 2021;11(7):1012. DOI: 10.3390/biom11071012
dc.identifier.issn 2218-273X
dc.identifier.uri http://hdl.handle.net/10230/48327
dc.description.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.
dc.description.sponsorship This work was supported by the Spanish Ministry of Science and Innovation and FEDER Funds through grants SAF2017-83372-R (FJM); RTI2018-094809-B-I00 (JMFF); PID2019-106755RB-I00 (RV); and through the “María de Maeztu” Programme for Units of Excellence in R&D (award CEX2018-000792-M).
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher MDPI
dc.relation.ispartof Biomolecules. 2021;11(7):1012
dc.rights © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
dc.rights.uri http://creativecommons.org/licenses/by/4.0/
dc.title Mitostasis, calcium and free radicals in health, aging and neurodegeneration
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.3390/biom11071012
dc.subject.keyword Aging
dc.subject.keyword Calcium
dc.subject.keyword Mitochondria
dc.subject.keyword Mitostasis
dc.subject.keyword Nitric oxide
dc.subject.keyword Oxidative stress
dc.relation.projectID info:eu-repo/grantAgreement/ES/2PE/SAF2017-83372-R
dc.relation.projectID info:eu-repo/grantAgreement/ES/2PE/RTI2018-094809-B-I00
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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