Mitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury
Mitochondria are organelles of eukaryotic cells delimited by two membranes and cristae that consume oxygen to produce adenosine triphosphate (ATP), and are involved in the synthesis of vital metabolites, calcium homeostasis, and cell death mechanisms. Strikingly, normal mitochondria function as an i...
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IMR Press
2025-01-01
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Series: | Journal of Integrative Neuroscience |
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Online Access: | https://www.imrpress.com/journal/JIN/24/1/10.31083/JIN25292 |
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author | Randhall Bruce Carteri |
author_facet | Randhall Bruce Carteri |
author_sort | Randhall Bruce Carteri |
collection | DOAJ |
description | Mitochondria are organelles of eukaryotic cells delimited by two membranes and cristae that consume oxygen to produce adenosine triphosphate (ATP), and are involved in the synthesis of vital metabolites, calcium homeostasis, and cell death mechanisms. Strikingly, normal mitochondria function as an integration center between multiple conditions that determine neural cell homeostasis, whereas lesions that lead to mitochondrial dysfunction can desynchronize cellular functions, thus contributing to the pathophysiology of traumatic brain injury (TBI). In addition, TBI leads to impaired coupling of the mitochondrial electron transport system with oxidative phosphorylation that provides most of the energy needed to maintain vital functions, ionic homeostasis, and membrane potentials. Furthermore, mitochondrial metabolism produces signaling molecules such as reactive oxygen species (ROS), regulating calcium levels and controlling the expression profile of intrinsic pro-apoptotic effectors influenced by TBI. Hence, the set of these functions is widely referred to as ‘mitochondrial function’, although the complexity of the relationship between such components limits such a definition. In this review, we present mitochondria as a therapeutic target, focus on TBI, and discuss aspects of mitochondrial structure and function. |
format | Article |
id | doaj-art-78c55e14c8244c61ad3b66a67b08faa9 |
institution | Kabale University |
issn | 0219-6352 1757-448X |
language | English |
publishDate | 2025-01-01 |
publisher | IMR Press |
record_format | Article |
series | Journal of Integrative Neuroscience |
spelling | doaj-art-78c55e14c8244c61ad3b66a67b08faa92025-01-25T07:38:07ZengIMR PressJournal of Integrative Neuroscience0219-63521757-448X2025-01-012412529210.31083/JIN25292S0219-6352(24)00844-1Mitochondria as a Therapeutic Target: Focusing on Traumatic Brain InjuryRandhall Bruce Carteri0Department of Hepatology, Federal University of Health Sciences of Porto Alegre (UFCSPA), 90050-170 Porto Alegre, Rio Grande do Sul (RS), BrazilMitochondria are organelles of eukaryotic cells delimited by two membranes and cristae that consume oxygen to produce adenosine triphosphate (ATP), and are involved in the synthesis of vital metabolites, calcium homeostasis, and cell death mechanisms. Strikingly, normal mitochondria function as an integration center between multiple conditions that determine neural cell homeostasis, whereas lesions that lead to mitochondrial dysfunction can desynchronize cellular functions, thus contributing to the pathophysiology of traumatic brain injury (TBI). In addition, TBI leads to impaired coupling of the mitochondrial electron transport system with oxidative phosphorylation that provides most of the energy needed to maintain vital functions, ionic homeostasis, and membrane potentials. Furthermore, mitochondrial metabolism produces signaling molecules such as reactive oxygen species (ROS), regulating calcium levels and controlling the expression profile of intrinsic pro-apoptotic effectors influenced by TBI. Hence, the set of these functions is widely referred to as ‘mitochondrial function’, although the complexity of the relationship between such components limits such a definition. In this review, we present mitochondria as a therapeutic target, focus on TBI, and discuss aspects of mitochondrial structure and function.https://www.imrpress.com/journal/JIN/24/1/10.31083/JIN25292metabolismneurodegenerationhead injury |
spellingShingle | Randhall Bruce Carteri Mitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury Journal of Integrative Neuroscience metabolism neurodegeneration head injury |
title | Mitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury |
title_full | Mitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury |
title_fullStr | Mitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury |
title_full_unstemmed | Mitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury |
title_short | Mitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury |
title_sort | mitochondria as a therapeutic target focusing on traumatic brain injury |
topic | metabolism neurodegeneration head injury |
url | https://www.imrpress.com/journal/JIN/24/1/10.31083/JIN25292 |
work_keys_str_mv | AT randhallbrucecarteri mitochondriaasatherapeutictargetfocusingontraumaticbraininjury |