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Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD)
Post-traumatic stress disorder (PTSD) is a neuropsychiatric disorder that occurs in approximately 15% of people as a result of some traumatic events. The main symptoms are re-experiencing and avoidance of everything related to this event and hyperarousal. The main component of the pathophysiology of...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10628526/ https://www.ncbi.nlm.nih.gov/pubmed/37942228 http://dx.doi.org/10.3389/fphys.2023.1222826 |
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author | Dmytriv, Tetiana R. Tsiumpala, Sviatoslav A. Semchyshyn, Halyna M. Storey, Kenneth B. Lushchak, Volodymyr I. |
author_facet | Dmytriv, Tetiana R. Tsiumpala, Sviatoslav A. Semchyshyn, Halyna M. Storey, Kenneth B. Lushchak, Volodymyr I. |
author_sort | Dmytriv, Tetiana R. |
collection | PubMed |
description | Post-traumatic stress disorder (PTSD) is a neuropsychiatric disorder that occurs in approximately 15% of people as a result of some traumatic events. The main symptoms are re-experiencing and avoidance of everything related to this event and hyperarousal. The main component of the pathophysiology of PTSD is an imbalance in the functioning of the hypothalamic-pituitary-adrenal axis (HPA) and development of neuroinflammation. In parallel with this, mitochondrial dysfunction is observed, as in many other diseases. In this review, we focus on the question how mitochondria may be involved in the development of neuroinflammation and its maintaining at PTSD. First, we describe the differences in the operation of the neuro-endocrine system during stress versus PTSD. We then show changes in the activity/expression of mitochondrial proteins in PTSD and how they can affect the levels of hormones involved in PTSD development, as well as how mitochondrial damage/pathogen-associated molecule patterns (DAMPs/PAMPs) trigger development of inflammation. In addition, we examine the possibility of treating PTSD-related inflammation using mitochondria as a target. |
format | Online Article Text |
id | pubmed-10628526 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-106285262023-11-08 Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD) Dmytriv, Tetiana R. Tsiumpala, Sviatoslav A. Semchyshyn, Halyna M. Storey, Kenneth B. Lushchak, Volodymyr I. Front Physiol Physiology Post-traumatic stress disorder (PTSD) is a neuropsychiatric disorder that occurs in approximately 15% of people as a result of some traumatic events. The main symptoms are re-experiencing and avoidance of everything related to this event and hyperarousal. The main component of the pathophysiology of PTSD is an imbalance in the functioning of the hypothalamic-pituitary-adrenal axis (HPA) and development of neuroinflammation. In parallel with this, mitochondrial dysfunction is observed, as in many other diseases. In this review, we focus on the question how mitochondria may be involved in the development of neuroinflammation and its maintaining at PTSD. First, we describe the differences in the operation of the neuro-endocrine system during stress versus PTSD. We then show changes in the activity/expression of mitochondrial proteins in PTSD and how they can affect the levels of hormones involved in PTSD development, as well as how mitochondrial damage/pathogen-associated molecule patterns (DAMPs/PAMPs) trigger development of inflammation. In addition, we examine the possibility of treating PTSD-related inflammation using mitochondria as a target. Frontiers Media S.A. 2023-10-24 /pmc/articles/PMC10628526/ /pubmed/37942228 http://dx.doi.org/10.3389/fphys.2023.1222826 Text en Copyright © 2023 Dmytriv, Tsiumpala, Semchyshyn, Storey and Lushchak. https://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 | Physiology Dmytriv, Tetiana R. Tsiumpala, Sviatoslav A. Semchyshyn, Halyna M. Storey, Kenneth B. Lushchak, Volodymyr I. Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD) |
title | Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD) |
title_full | Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD) |
title_fullStr | Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD) |
title_full_unstemmed | Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD) |
title_short | Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD) |
title_sort | mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (ptsd) |
topic | Physiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10628526/ https://www.ncbi.nlm.nih.gov/pubmed/37942228 http://dx.doi.org/10.3389/fphys.2023.1222826 |
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