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ER–mitochondria signaling in Parkinson’s disease
Mitochondria form close physical contacts with a specialized domain of the endoplasmic reticulum (ER), known as the mitochondria-associated membrane (MAM). This association constitutes a key signaling hub to regulate several fundamental cellular processes. Alterations in ER–mitochondria signaling ha...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5832754/ https://www.ncbi.nlm.nih.gov/pubmed/29497039 http://dx.doi.org/10.1038/s41419-017-0079-3 |
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author | Gómez-Suaga, Patricia Bravo-San Pedro, José M González-Polo, Rosa A. Fuentes, José M. Niso-Santano, Mireia |
author_facet | Gómez-Suaga, Patricia Bravo-San Pedro, José M González-Polo, Rosa A. Fuentes, José M. Niso-Santano, Mireia |
author_sort | Gómez-Suaga, Patricia |
collection | PubMed |
description | Mitochondria form close physical contacts with a specialized domain of the endoplasmic reticulum (ER), known as the mitochondria-associated membrane (MAM). This association constitutes a key signaling hub to regulate several fundamental cellular processes. Alterations in ER–mitochondria signaling have pleiotropic effects on a variety of intracellular events resulting in mitochondrial damage, Ca(2+) dyshomeostasis, ER stress and defects in lipid metabolism and autophagy. Intriguingly, many of these cellular processes are perturbed in neurodegenerative diseases. Furthermore, increasing evidence highlights that ER–mitochondria signaling contributes to these diseases, including Parkinson’s disease (PD). PD is the second most common neurodegenerative disorder, for which effective mechanism-based treatments remain elusive. Several PD-related proteins localize at mitochondria or MAM and have been shown to participate in ER–mitochondria signaling regulation. Likewise, PD-related mutations have been shown to damage this signaling. Could ER–mitochondria associations be the link between pathogenic mechanisms involved in PD, providing a common mechanism? Would this provide a pharmacological target for treating this devastating disease? In this review, we aim to summarize the current knowledge of ER–mitochondria signaling and the recent evidence concerning damage to this signaling in PD. |
format | Online Article Text |
id | pubmed-5832754 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58327542018-03-05 ER–mitochondria signaling in Parkinson’s disease Gómez-Suaga, Patricia Bravo-San Pedro, José M González-Polo, Rosa A. Fuentes, José M. Niso-Santano, Mireia Cell Death Dis Review Article Mitochondria form close physical contacts with a specialized domain of the endoplasmic reticulum (ER), known as the mitochondria-associated membrane (MAM). This association constitutes a key signaling hub to regulate several fundamental cellular processes. Alterations in ER–mitochondria signaling have pleiotropic effects on a variety of intracellular events resulting in mitochondrial damage, Ca(2+) dyshomeostasis, ER stress and defects in lipid metabolism and autophagy. Intriguingly, many of these cellular processes are perturbed in neurodegenerative diseases. Furthermore, increasing evidence highlights that ER–mitochondria signaling contributes to these diseases, including Parkinson’s disease (PD). PD is the second most common neurodegenerative disorder, for which effective mechanism-based treatments remain elusive. Several PD-related proteins localize at mitochondria or MAM and have been shown to participate in ER–mitochondria signaling regulation. Likewise, PD-related mutations have been shown to damage this signaling. Could ER–mitochondria associations be the link between pathogenic mechanisms involved in PD, providing a common mechanism? Would this provide a pharmacological target for treating this devastating disease? In this review, we aim to summarize the current knowledge of ER–mitochondria signaling and the recent evidence concerning damage to this signaling in PD. Nature Publishing Group UK 2018-03-01 /pmc/articles/PMC5832754/ /pubmed/29497039 http://dx.doi.org/10.1038/s41419-017-0079-3 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Review Article Gómez-Suaga, Patricia Bravo-San Pedro, José M González-Polo, Rosa A. Fuentes, José M. Niso-Santano, Mireia ER–mitochondria signaling in Parkinson’s disease |
title | ER–mitochondria signaling in Parkinson’s disease |
title_full | ER–mitochondria signaling in Parkinson’s disease |
title_fullStr | ER–mitochondria signaling in Parkinson’s disease |
title_full_unstemmed | ER–mitochondria signaling in Parkinson’s disease |
title_short | ER–mitochondria signaling in Parkinson’s disease |
title_sort | er–mitochondria signaling in parkinson’s disease |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5832754/ https://www.ncbi.nlm.nih.gov/pubmed/29497039 http://dx.doi.org/10.1038/s41419-017-0079-3 |
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