ReviewOxidative medicine and cellular longevity2022
Mitophagy in Traumatic Brain Injury: A New Target for Therapeutic Intervention.
Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 29 citations in OpenAlex.
- Pathophysiological mechanisms of post-exertional malaise: an integrative analysis based on the metabolism-immune-neuro interaction model.Frontiers in immunology · 2026Pooled it
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- Old and Promising Markers Related to Autophagy in Traumatic Brain Injury.International journal of molecular sciences · 2022Pooled it
- Mitochondrial Dysfunction in Traumatic Brain Injury and Its Theranostic Implications.Biomolecules · 2026Review
- Transcutaneous Auricular Vagus Nerve Stimulation Alleviates Oxidative Stress and Improves Neurological Outcomes After Traumatic Brain Injury in Mice.CNS neuroscience & therapeutics · 2026Article
- Zipper-interacting Protein Kinase Modulates Gene Expression Linked to Synaptic and Neuronal Processes after Traumatic Brain Injury.Molecular neurobiology · 2026Article
- Astrocyte-derived Exosomal GJA1-20 k Targets Pink1-mediated Mitophagy to Attenuate Traumatic Brain Injury.Translational stroke research · 2025Article
- Mitophagy in Brain Injuries: Mechanisms, Roles, and Therapeutic Potential.Molecular neurobiology · 2025Review
- Copper aggravated synaptic damage after traumatic brain injury by downregulating BNIP3-mediated mitophagy.Autophagy · 2025Article
- Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Luteolin attenuates LPS-induced damage in IPEC-J2 cells by enhancing mitophagy via AMPK signaling pathway activation.Frontiers in nutrition · 2025Article
- Therapeutic Effect of Donepezil on Neuroinflammation and Cognitive Impairment after Moderate Traumatic Brain Injury.Life (Basel, Switzerland) · 2024Article
- Role of mitochondrial dysfunction in acute traumatic brain injury: Evidence from bioinformatics analysis.Heliyon · 2024Article
- Erianin promotes endogenous neurogenesis in traumatic brain injury rats.Scientific reports · 2024Article
- p17/C18-ceramide-mediated mitophagy is an endogenous neuroprotective response in preclinical and clinical brain injury.PNAS nexus · 2024Article
- Enhancing mitophagy by ligustilide through BNIP3-LC3 interaction attenuates oxidative stress-induced neuronal apoptosis in spinal cord injury.International journal of biological sciences · 2024Article
- Intranasal nerve growth factor for prevention and recovery of the outcomes of traumatic brain injury.Neural regeneration research · 2023Review
- Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials.Oxidative medicine and cellular longevity · 2023Review
- [Advances of the role of mitochondrial dysfunction in the spinal cord injury and its relevant treatments].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) contributes to death, and disability worldwide more than any other traumatic insult and damage to cellular components including mitochondria leads to the impairment of cellular functions and brain function. In neurons, mitophagy, autophagy-mediated degradation of damaged mitochondria, is a key process in cellular quality control including mitochondrial homeostasis and energy supply and plays a fundamental role in neuronal survival and health. Conversely, defective mitophagy leads to the accumulation of damaged mitochondria and cellular dysfunction, contributing to inflammation, oxidative stress, and neuronal cell death. Therefore, an extensive characterization of mitophagy-related protective mechanisms, taking into account the complex mechanisms by which each molecular player is connected to the others, may provide a rationale for the development of new therapeutic strategies in TBI patients. Here, we discuss the contribution of defective mitophagy in TBI, and the underlying molecular mechanisms of mitophagy in inflammation, oxidative stress, and neuronal cell death highlight novel therapeutics based on newly discovered mitophagy-inducing strategies.
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What OpenQuestion holds
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.