ArticleHeliyon2024
Role of mitochondrial dysfunction in acute traumatic brain injury: Evidence from bioinformatics analysis.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed.
- The mitochondrial epigenome and noncoding genome in aging and brain diseases.Trends in neurosciences · 2026Review
- Mitochondrial Dysfunction in Traumatic Brain Injury and Its Theranostic Implications.Biomolecules · 2026Review
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.Experimental neurology · 2026Article
- Association between Neutrophil-to-Albumin Ratio and 28-Day All-Cause Mortality in Patients with Traumatic Brain Injury : A Retrospective Analysis of the MIMIC-IV Database.Journal of Korean Neurosurgical Society · 2025Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- T Cell Involvement in Neuroinflammation After Traumatic Brain Injury: Implications for Therapeutic Intervention.CNS neuroscience & therapeutics · 2025Review
- Mitochondrial and ER stress crosstalk in TBI: mechanistic insights and therapeutic opportunities.Frontiers in cellular neuroscience · 2025Review
- The Mechanism of Action of the Active Ingredients ofViruses · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The intricate regulatory relationship between mitochondrial dysfunction, apoptosis, and immune cells remains largely elusive following traumatic brain injury (TBI). Methods: The GSE45997 dataset from the Gene Expression Omnibus database and utilized GEO2R to screen for differentially expressed genes (DEGs). Functional enrichment analyses were performed. Mitochondrial gene data from the MitoCarta3.0 database were combined with the DEGs to identify mitochondria-related DEGs (MitoDEGs). The hub MitoDEGs related to apoptosis were further screened. Animal models of TBI were established to investigate the mechanisms underlying mitochondrial dysfunction regulation of apoptosis. Furthermore, we explored the relationship between MitoDEGs/hub MitoDEGs and immune cells using the Spearman correlation method. Results: Fifty-seven MitoDEGs were significantly enriched in pathways related to fatty acid degradation and metabolism. We identified three upregulated hub MitoDEGs, namely Conclusions: This study sheds light on enhanced fatty acid metabolism following mitochondrial dysfunction and its potential association with apoptosis and immune cell activation, thereby providing new mechanistic insights into the acute phase of TBI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.