ArticleJournal of neurotrauma2019
Proteomic Analysis and Biochemical Correlates of Mitochondrial Dysfunction after Low-Intensity Primary Blast Exposure.
Article in Journal of neurotrauma, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- PDE5 inhibition restores mitochondrial function and improves neurobehavioral outcomes after repeated mild blast TBI.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Restoring mitochondrial health after blast-induced traumatic brain injury: modifiable factors and therapeutic opportunities.npj metabolic health and disease · 2026Review
- Comparison of explosively driven shock tube and open-air blast wave propagation.Scientific reports · 2026Article
- Sex and Genotype Affect Mouse Hippocampal Gene Expression in Response to Blast-Induced Traumatic Brain Injury.Molecular neurobiology · 2025Article
- Assessment model of blast injury: A narrative review.iScience · 2025Review
- Mitochondrial proteome landscape unveils key insights into melanoma severity and treatment strategies.Cancer · 2025Article
- A Systematic Review of Traumatic Brain Injury in Modern Rodent Models: Current Status and Future Prospects.Biology · 2024Review
- Modeling Highly Repetitive Low-level Blast Exposure in Mice.Journal of visualized experiments : JoVE · 2024Article
- Quantitative proteomic profiling in brain subregions of mice exposed to open-field low-intensity blast reveals position-dependent blast effects.Shock waves · 2024Article
- The Chronic Effects of a Single Low-Intensity Blast Exposure on Phosphoproteome Networks and Cognitive Function Influenced by Mutant Tau Overexpression.International journal of molecular sciences · 2024Article
- The role of mitochondrial uncoupling in the regulation of mitostasis after traumatic brain injury.Neurochemistry international · 2024Article
- Applying Proteomics and Computational Approaches to Identify Novel Targets in Blast-Associated Post-Traumatic Epilepsy.International journal of molecular sciences · 2024Article
- Individualized high-resolution analysis to categorize diverse learning and memory deficits in tau rTg4510 mice exposed to low-intensity blast.Frontiers in cellular neuroscience · 2024Article
- Blast-related mild TBI: LIMBIC-CENC focused review with implications commentary.NeuroRehabilitation · 2024Review
- Low-Intensity Blast Exposure Induces Multifaceted Long-Lasting Anxiety-Related Behaviors in Mice.Neurotrauma reports · 2024Article
- An overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms.Frontiers in cellular neuroscience · 2024Review
- Quantitative proteomic and phosphoproteomic analyses of the hippocampus reveal the involvement of NMDAR1 signaling in repetitive mild traumatic brain injury.Neural regeneration research · 2023Article
- Mitochondrial Dysfunction After Repeated Mild Blast Traumatic Brain Injury Is Attenuated by a Mild Mitochondrial Uncoupling Prodrug.Journal of neurotrauma · 2023Article
- Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice.Acta neuropathologica communications · 2023Article
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
Abstract
Service members during military actions or combat training are frequently exposed to primary blasts by weaponry. Most studies have investigated moderate or severe brain injuries from blasts generating overpressures >100 kPa, whereas understanding the pathophysiology of low-intensity blast (LIB)-induced mild traumatic brain injury (mTBI) leading to neurological deficits remains elusive. Our recent studies, using an open-field LIB-induced mTBI mouse model with a peak overpressure at 46.6 kPa, demonstrated behavioral impairments and brain nanoscale damages, notably mitochondrial and axonal ultrastructural changes. In this study, we used tandem mass tagged (TMT) quantitative proteomics and bioinformatics analysis to seek insights into the molecular mechanisms underlying ultrastructural pathology. Changes in global- and phospho-proteomes were determined at 3 and 24 h and at 7 and 30 days post injury (DPI), in order to investigate the biochemical and molecular correlates of mitochondrial dysfunction. Results showed striking dynamic changes in a total of 2216 proteins and 459 phosphorylated proteins at vary time points after blast. Disruption of key canonical pathways included evidence of mitochondrial dysfunction, oxidative stress, axonal/cytoskeletal/synaptic dysregulation, and neurodegeneration. Bioinformatic analysis identified blast-induced trends in networks related to cellular growth/development/movement/assembly and cell-to-cell signaling interactions. With observations of proteomic changes, we found LIB-induced oxidative stress associated with mitochondrial dysfunction mainly at 7 and 30 DPI. These dysfunctions included impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated respiration-relevant enzyme activities. Insights on the early pathogenesis of primary LIB-induced brain damage provide a template for further characterization of its chronic effects, identification of potential biomarkers, and targets for intervention.
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Registered trials
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