Mitochondrial Dysfunction in Neurodegeneration: A Translational Perspective

Dear Colleagues,

Mitochondria after traumatic brain injury (TBI) have emerged as a focal point in translational research, with their pivotal role in the pathophysiology of TBI being demonstrated. These cellular powerhouses play a multifaceted role in energy production, calcium homeostasis, and cell survival, making them susceptible to dysfunction following TBI.

Studies have revealed that TBI triggers a cascade of events leading to mitochondrial dysfunction. The disruption of mitochondrial membrane potential, impaired oxidative phosphorylation, and excessive reactive oxygen species (ROS) production contribute to energy depletion and oxidative stress, exacerbating neuronal damage. Mitochondrial DNA damage and altered mitochondrial dynamics further exacerbate the dysfunction, leading to a vicious cycle of neuronal death and inflammation.

Furthermore, understanding the intricate interplay between mitochondrial dysfunction and other secondary injury mechanisms, such as neuroinflammation and excitotoxicity, is crucial for developing comprehensive therapeutic strategies. Mitochondria serve as a convergence point for various pathways involved in TBI pathology, making them an attractive target for translational research.

This Special Issue aims to address the current trend in translational research, focusing on mitochondrial dysfunction after TBI by unraveling the underlying mechanisms and exploring potential therapeutic interventions as well as addressing technological advancements in the field, with the hope of ultimately improving outcomes and advancing clinical management in TBI patients.

Dr. Hemendra Vekaria
Guest Editor

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• mitochondrial dysfunction
• traumatic brain injury
• secondary damage
• bioenergetics