Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?

Calcium (Ca 2+ ) is a versatile secondary messenger involved in the regulation of a plethora of different signaling pathways for cell maintenance. Specifically, intracellular Ca 2+ homeostasis is mainly regulated by the endoplasmic reticulum and the mitochondria, whose Ca 2+ exchange is mediated by...

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Autores: Rodríguez LR, Lapeña-Luzón T, Benetó N, Beltran-Beltran V, Pallardó FV, Gonzalez-Cabo P, Navarro JA
Formato: artículo
Estado:Versión publicada
Fecha de publicación:2022
País:España
Recursos:Centro de Investigación Principe Felipe (CIPF)
Repositorio:r-CIPF. Repositorio Institucional Producción Científica del Centro de Investigación Principe Felipe (CIPF)
OAI Identifier:oai:cipf.fundanetsuite.com:p4045
Acesso em linha:https://cipf.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=4045
Access Level:acceso abierto
Palavra-chave:Charcot–Marie–Tooth, Friedreich’s ataxia, amyotrophic lateral sclerosis, calcium, endoplasmic reticulum, mitochondria, mitochondrial calcium uniporter, neurological, sigma-1 receptor
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spelling Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?Rodríguez LRLapeña-Luzón TBenetó NBeltran-Beltran VPallardó FVGonzalez-Cabo PNavarro JACharcot–Marie–Tooth, Friedreich’s ataxia, amyotrophic lateral sclerosis, calcium, endoplasmic reticulum, mitochondria, mitochondrial calcium uniporter, neurological, sigma-1 receptorCalcium (Ca 2+ ) is a versatile secondary messenger involved in the regulation of a plethora of different signaling pathways for cell maintenance. Specifically, intracellular Ca 2+ homeostasis is mainly regulated by the endoplasmic reticulum and the mitochondria, whose Ca 2+ exchange is mediated by appositions, termed endoplasmic reticulum-mitochondria-associated membranes (MAMs), formed by proteins resident in both compartments. These tethers are essential to manage the mitochondrial Ca 2+ influx that regulates the mitochondrial function of bioenergetics, mitochondrial dynamics, cell death, and oxidative stress. However, alterations of these pathways lead to the development of multiple human diseases, including neurological disorders, such as amyotrophic lateral sclerosis, Friedreich's ataxia, and Charcot-Marie-Tooth. A common hallmark in these disorders is mitochondrial dysfunction, associated with abnormal mitochondrial Ca 2+ handling that contributes to neurodegeneration. In this work, we highlight the importance of Ca 2+ signaling in mitochondria and how the mechanism of communication in MAMs is pivotal for mitochondrial maintenance and cell homeostasis. Lately, we outstand potential targets located in MAMs by addressing different therapeutic strategies focused on restoring mitochondrial Ca 2+ uptake as an emergent approach for neurological diseases.MDPI2022info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://cipf.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=4045AntioxidantsISSN: 20763921reponame:r-CIPF. Repositorio Institucional Producción Científica del Centro de Investigación Principe Felipe (CIPF)instname:Centro de Investigación Principe Felipe (CIPF)Inglésinfo:eu-repo/semantics/openAccessoai:cipf.fundanetsuite.com:p40452026-06-17T11:19:47Z
dc.title.none.fl_str_mv Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?
title Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?
spellingShingle Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?
Rodríguez LR
Charcot–Marie–Tooth, Friedreich’s ataxia, amyotrophic lateral sclerosis, calcium, endoplasmic reticulum, mitochondria, mitochondrial calcium uniporter, neurological, sigma-1 receptor
title_short Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?
title_full Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?
title_fullStr Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?
title_full_unstemmed Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?
title_sort Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?
dc.creator.none.fl_str_mv Rodríguez LR
Lapeña-Luzón T
Benetó N
Beltran-Beltran V
Pallardó FV
Gonzalez-Cabo P
Navarro JA
author Rodríguez LR
author_facet Rodríguez LR
Lapeña-Luzón T
Benetó N
Beltran-Beltran V
Pallardó FV
Gonzalez-Cabo P
Navarro JA
author_role author
author2 Lapeña-Luzón T
Benetó N
Beltran-Beltran V
Pallardó FV
Gonzalez-Cabo P
Navarro JA
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Charcot–Marie–Tooth, Friedreich’s ataxia, amyotrophic lateral sclerosis, calcium, endoplasmic reticulum, mitochondria, mitochondrial calcium uniporter, neurological, sigma-1 receptor
topic Charcot–Marie–Tooth, Friedreich’s ataxia, amyotrophic lateral sclerosis, calcium, endoplasmic reticulum, mitochondria, mitochondrial calcium uniporter, neurological, sigma-1 receptor
description Calcium (Ca 2+ ) is a versatile secondary messenger involved in the regulation of a plethora of different signaling pathways for cell maintenance. Specifically, intracellular Ca 2+ homeostasis is mainly regulated by the endoplasmic reticulum and the mitochondria, whose Ca 2+ exchange is mediated by appositions, termed endoplasmic reticulum-mitochondria-associated membranes (MAMs), formed by proteins resident in both compartments. These tethers are essential to manage the mitochondrial Ca 2+ influx that regulates the mitochondrial function of bioenergetics, mitochondrial dynamics, cell death, and oxidative stress. However, alterations of these pathways lead to the development of multiple human diseases, including neurological disorders, such as amyotrophic lateral sclerosis, Friedreich's ataxia, and Charcot-Marie-Tooth. A common hallmark in these disorders is mitochondrial dysfunction, associated with abnormal mitochondrial Ca 2+ handling that contributes to neurodegeneration. In this work, we highlight the importance of Ca 2+ signaling in mitochondria and how the mechanism of communication in MAMs is pivotal for mitochondrial maintenance and cell homeostasis. Lately, we outstand potential targets located in MAMs by addressing different therapeutic strategies focused on restoring mitochondrial Ca 2+ uptake as an emergent approach for neurological diseases.
publishDate 2022
dc.date.none.fl_str_mv 2022
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://cipf.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=4045
url https://cipf.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=4045
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv Antioxidants
ISSN: 20763921
reponame:r-CIPF. Repositorio Institucional Producción Científica del Centro de Investigación Principe Felipe (CIPF)
instname:Centro de Investigación Principe Felipe (CIPF)
instname_str Centro de Investigación Principe Felipe (CIPF)
reponame_str r-CIPF. Repositorio Institucional Producción Científica del Centro de Investigación Principe Felipe (CIPF)
collection r-CIPF. Repositorio Institucional Producción Científica del Centro de Investigación Principe Felipe (CIPF)
repository.name.fl_str_mv
repository.mail.fl_str_mv
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