Post-traumatic stress disorder (PTSD) is a devastating mental condition that affects millions of people worldwide. PTSD is caused by exposure to traumatic events that may include exposure to different forms of direct violence resulting in death, serious injury or sexual violence, as well as indirect but repeated assaults of trauma. PTSD symptoms include terrifying and realistic flashbacks of war scenes, intrusive memories of the trauma, panic, inability to sleep and nightmares, and avoidance of anything that resembles the trauma. While the cause of PTSD is clear, the underlying cellular/molecular mechanisms remain elusive. Identifying the mechanisms involved in PTSD pathophysiology is necessary for the appropriate management and prevention of this disorder.
Traumatic experiences from conflicts experienced by civilians and military personnel exposed to the warzone dramatically increase the incidence of PTSD. Therefore, there is a need to focus on developing preventive approaches, diagnostic biomarkers and treatment strategies targeting intracellular/molecular triggers specifically in military populations which have shown to be pharmaco-resistant. It is well known that mitochondrial dysfunction is an important trigger of different mental disorders, including depression and anxiety. Although PTSD mechanisms are understudied, it is established that mitochondria, for example, play a key role in synaptic neurotransmitter signaling and neuron cell death. In the same way, metabolic mismatch as well as redox imbalance may occur during the first stage of the cellular stress response. When the response persists abnormally, chronic disorders can develop due to altered content of mitochondrial and cellular macromolecules, including stress granule formation and changes in contact sites between different organelles. Thus, the understanding of mitochondria-mediated cellular response to stress factors, and its manifestation at different levels of organization, is crucial for efficient treatment of a broad array of chronic, developmental, autoimmune, and degenerative disorders, including PTSD.
The aim of the proposed Research Topic, “Role of mitochondria in Post-Traumatic Stress Disorder (PTSD)”, is to present mitochondria-mediated cellular stress response by highlighting homeostasis and pathology progression , and discuss possible interventions targeting mitochondrial function to uncover new biomarker candidates. The collections of this work are to provide novel and in depth knowledge on PTSD neurobiological mechanisms and furnish new treatment approaches to mitigate PTSD through studies in animal models. Ultimately, the translation of this work to humans affected by PTSD and the use of targeted strategies and prophylactic approaches to treat and prevent the severity of the disorder would advance this field. In this Research Topic, original research articles and reviews are welcome. We look forward to your contributions in this timely line of research.
Post-traumatic stress disorder (PTSD) is a devastating mental condition that affects millions of people worldwide. PTSD is caused by exposure to traumatic events that may include exposure to different forms of direct violence resulting in death, serious injury or sexual violence, as well as indirect but repeated assaults of trauma. PTSD symptoms include terrifying and realistic flashbacks of war scenes, intrusive memories of the trauma, panic, inability to sleep and nightmares, and avoidance of anything that resembles the trauma. While the cause of PTSD is clear, the underlying cellular/molecular mechanisms remain elusive. Identifying the mechanisms involved in PTSD pathophysiology is necessary for the appropriate management and prevention of this disorder.
Traumatic experiences from conflicts experienced by civilians and military personnel exposed to the warzone dramatically increase the incidence of PTSD. Therefore, there is a need to focus on developing preventive approaches, diagnostic biomarkers and treatment strategies targeting intracellular/molecular triggers specifically in military populations which have shown to be pharmaco-resistant. It is well known that mitochondrial dysfunction is an important trigger of different mental disorders, including depression and anxiety. Although PTSD mechanisms are understudied, it is established that mitochondria, for example, play a key role in synaptic neurotransmitter signaling and neuron cell death. In the same way, metabolic mismatch as well as redox imbalance may occur during the first stage of the cellular stress response. When the response persists abnormally, chronic disorders can develop due to altered content of mitochondrial and cellular macromolecules, including stress granule formation and changes in contact sites between different organelles. Thus, the understanding of mitochondria-mediated cellular response to stress factors, and its manifestation at different levels of organization, is crucial for efficient treatment of a broad array of chronic, developmental, autoimmune, and degenerative disorders, including PTSD.
The aim of the proposed Research Topic, “Role of mitochondria in Post-Traumatic Stress Disorder (PTSD)”, is to present mitochondria-mediated cellular stress response by highlighting homeostasis and pathology progression , and discuss possible interventions targeting mitochondrial function to uncover new biomarker candidates. The collections of this work are to provide novel and in depth knowledge on PTSD neurobiological mechanisms and furnish new treatment approaches to mitigate PTSD through studies in animal models. Ultimately, the translation of this work to humans affected by PTSD and the use of targeted strategies and prophylactic approaches to treat and prevent the severity of the disorder would advance this field. In this Research Topic, original research articles and reviews are welcome. We look forward to your contributions in this timely line of research.
