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ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective

The mitochondrial and endoplasmic reticulum (ER) homeostasis is pivotal to the maintenance of an array of physiological processes. The physical contact and association between ER and mitochondria, known as the ER–mitochondria microdomains or mitochondria-associated ER membrane (MAM), temporally and...

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Autores principales: Zhou, Hao, Wang, Shuyi, Hu, Shunying, Chen, Yundai, Ren, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6013587/
https://www.ncbi.nlm.nih.gov/pubmed/29962971
http://dx.doi.org/10.3389/fphys.2018.00755
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author Zhou, Hao
Wang, Shuyi
Hu, Shunying
Chen, Yundai
Ren, Jun
author_facet Zhou, Hao
Wang, Shuyi
Hu, Shunying
Chen, Yundai
Ren, Jun
author_sort Zhou, Hao
collection PubMed
description The mitochondrial and endoplasmic reticulum (ER) homeostasis is pivotal to the maintenance of an array of physiological processes. The physical contact and association between ER and mitochondria, known as the ER–mitochondria microdomains or mitochondria-associated ER membrane (MAM), temporally and spatially regulates the mitochondria/ER structure and function. More evidence suggests a role for MAMs in energy production, cellular contraction and mobility, and normal extracellular signal transmission. In pathological states, such as cardiac ischemia–reperfusion (I/R injury), this ER–mitochondria microdomains may act to participate in the cellular redox imbalance, ER stress, mitochondrial injury, energy deletion, and programmed cell death. From a therapeutic perspective, a better understanding of the cellular and molecular mechanisms of the pathogenic ER–mitochondria contact should help to identify potential therapeutic target for cardiac I/R injury and other cardiovascular diseases and also pave the road to new treatment modalities pertinent for the treatment of reperfusion damage in clinical practice. This review will mainly focus on the possible signaling pathways involved in the regulation of the ER–mitochondria contact. In particular, we will summarize the downstream signaling modalities influenced by ER–mitochondria microdomains, for example, mitochondrial fission, mitophagy, calcium balance, oxidative stress, and programmed cell death in details.
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spelling pubmed-60135872018-06-29 ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective Zhou, Hao Wang, Shuyi Hu, Shunying Chen, Yundai Ren, Jun Front Physiol Physiology The mitochondrial and endoplasmic reticulum (ER) homeostasis is pivotal to the maintenance of an array of physiological processes. The physical contact and association between ER and mitochondria, known as the ER–mitochondria microdomains or mitochondria-associated ER membrane (MAM), temporally and spatially regulates the mitochondria/ER structure and function. More evidence suggests a role for MAMs in energy production, cellular contraction and mobility, and normal extracellular signal transmission. In pathological states, such as cardiac ischemia–reperfusion (I/R injury), this ER–mitochondria microdomains may act to participate in the cellular redox imbalance, ER stress, mitochondrial injury, energy deletion, and programmed cell death. From a therapeutic perspective, a better understanding of the cellular and molecular mechanisms of the pathogenic ER–mitochondria contact should help to identify potential therapeutic target for cardiac I/R injury and other cardiovascular diseases and also pave the road to new treatment modalities pertinent for the treatment of reperfusion damage in clinical practice. This review will mainly focus on the possible signaling pathways involved in the regulation of the ER–mitochondria contact. In particular, we will summarize the downstream signaling modalities influenced by ER–mitochondria microdomains, for example, mitochondrial fission, mitophagy, calcium balance, oxidative stress, and programmed cell death in details. Frontiers Media S.A. 2018-06-15 /pmc/articles/PMC6013587/ /pubmed/29962971 http://dx.doi.org/10.3389/fphys.2018.00755 Text en Copyright © 2018 Zhou, Wang, Hu, Chen and Ren. 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 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 Physiology
Zhou, Hao
Wang, Shuyi
Hu, Shunying
Chen, Yundai
Ren, Jun
ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective
title ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective
title_full ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective
title_fullStr ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective
title_full_unstemmed ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective
title_short ER–Mitochondria Microdomains in Cardiac Ischemia–Reperfusion Injury: A Fresh Perspective
title_sort er–mitochondria microdomains in cardiac ischemia–reperfusion injury: a fresh perspective
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6013587/
https://www.ncbi.nlm.nih.gov/pubmed/29962971
http://dx.doi.org/10.3389/fphys.2018.00755
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