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When Friendship Turns Sour: Effective Communication Between Mitochondria and Intracellular Organelles in Parkinson's Disease
Parkinson's disease (PD) is a complex neurodegenerative disease with pathological hallmarks including progressive neuronal loss from the substantia nigra pars compacta and α-synuclein intraneuronal inclusions, known as Lewy bodies. Although the etiology of PD remains elusive, mitochondrial dama...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7733999/ https://www.ncbi.nlm.nih.gov/pubmed/33330511 http://dx.doi.org/10.3389/fcell.2020.607392 |
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author | Lin, Tsu-Kung Lin, Kai-Jung Lin, Kai-Lieh Liou, Chia-Wei Chen, Shang-Der Chuang, Yao-Chung Wang, Pei-Wen Chuang, Jiin-Haur Wang, Tzu-Jou |
author_facet | Lin, Tsu-Kung Lin, Kai-Jung Lin, Kai-Lieh Liou, Chia-Wei Chen, Shang-Der Chuang, Yao-Chung Wang, Pei-Wen Chuang, Jiin-Haur Wang, Tzu-Jou |
author_sort | Lin, Tsu-Kung |
collection | PubMed |
description | Parkinson's disease (PD) is a complex neurodegenerative disease with pathological hallmarks including progressive neuronal loss from the substantia nigra pars compacta and α-synuclein intraneuronal inclusions, known as Lewy bodies. Although the etiology of PD remains elusive, mitochondrial damage has been established to take center stage in the pathogenesis of PD. Mitochondria are critical to cellular energy production, metabolism, homeostasis, and stress responses; the association with PD emphasizes the importance of maintenance of mitochondrial network integrity. To accomplish the pleiotropic functions, mitochondria are dynamic not only within their own network but also in orchestrated coordination with other organelles in the cellular community. Through physical contact sites, signal transduction, and vesicle transport, mitochondria and intracellular organelles achieve the goals of calcium homeostasis, redox homeostasis, protein homeostasis, autophagy, and apoptosis. Herein, we review the finely tuned interactions between mitochondria and surrounding intracellular organelles, with focus on the nucleus, endoplasmic reticulum, Golgi apparatus, peroxisomes, and lysosomes. Participants that may contribute to the pathogenic mechanisms of PD will be highlighted in this review. |
format | Online Article Text |
id | pubmed-7733999 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-77339992020-12-15 When Friendship Turns Sour: Effective Communication Between Mitochondria and Intracellular Organelles in Parkinson's Disease Lin, Tsu-Kung Lin, Kai-Jung Lin, Kai-Lieh Liou, Chia-Wei Chen, Shang-Der Chuang, Yao-Chung Wang, Pei-Wen Chuang, Jiin-Haur Wang, Tzu-Jou Front Cell Dev Biol Cell and Developmental Biology Parkinson's disease (PD) is a complex neurodegenerative disease with pathological hallmarks including progressive neuronal loss from the substantia nigra pars compacta and α-synuclein intraneuronal inclusions, known as Lewy bodies. Although the etiology of PD remains elusive, mitochondrial damage has been established to take center stage in the pathogenesis of PD. Mitochondria are critical to cellular energy production, metabolism, homeostasis, and stress responses; the association with PD emphasizes the importance of maintenance of mitochondrial network integrity. To accomplish the pleiotropic functions, mitochondria are dynamic not only within their own network but also in orchestrated coordination with other organelles in the cellular community. Through physical contact sites, signal transduction, and vesicle transport, mitochondria and intracellular organelles achieve the goals of calcium homeostasis, redox homeostasis, protein homeostasis, autophagy, and apoptosis. Herein, we review the finely tuned interactions between mitochondria and surrounding intracellular organelles, with focus on the nucleus, endoplasmic reticulum, Golgi apparatus, peroxisomes, and lysosomes. Participants that may contribute to the pathogenic mechanisms of PD will be highlighted in this review. Frontiers Media S.A. 2020-11-30 /pmc/articles/PMC7733999/ /pubmed/33330511 http://dx.doi.org/10.3389/fcell.2020.607392 Text en Copyright © 2020 Lin, Lin, Lin, Liou, Chen, Chuang, Wang, Chuang and Wang. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cell and Developmental Biology Lin, Tsu-Kung Lin, Kai-Jung Lin, Kai-Lieh Liou, Chia-Wei Chen, Shang-Der Chuang, Yao-Chung Wang, Pei-Wen Chuang, Jiin-Haur Wang, Tzu-Jou When Friendship Turns Sour: Effective Communication Between Mitochondria and Intracellular Organelles in Parkinson's Disease |
title | When Friendship Turns Sour: Effective Communication Between Mitochondria and Intracellular Organelles in Parkinson's Disease |
title_full | When Friendship Turns Sour: Effective Communication Between Mitochondria and Intracellular Organelles in Parkinson's Disease |
title_fullStr | When Friendship Turns Sour: Effective Communication Between Mitochondria and Intracellular Organelles in Parkinson's Disease |
title_full_unstemmed | When Friendship Turns Sour: Effective Communication Between Mitochondria and Intracellular Organelles in Parkinson's Disease |
title_short | When Friendship Turns Sour: Effective Communication Between Mitochondria and Intracellular Organelles in Parkinson's Disease |
title_sort | when friendship turns sour: effective communication between mitochondria and intracellular organelles in parkinson's disease |
topic | Cell and Developmental Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7733999/ https://www.ncbi.nlm.nih.gov/pubmed/33330511 http://dx.doi.org/10.3389/fcell.2020.607392 |
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