ReviewMolecular neurobiology2015
Interactions of oxidative stress and neurovascular inflammation in the pathogenesis of traumatic brain injury.
Review in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers.
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Who cites it
229 citing papers in PubMed, 451 citations in OpenAlex.
- Pharmacological Modulation of Catecholaminergic Brain Injury by Dapagliflozin and Its Nanovesicular Formulation in an Isoproterenol Model.Journal of biochemical and molecular toxicology · 2026Article
- The crosstalk between blood-brain barrier and neural cells: bidirectional regulation of brain function and pathology.Biochemistry and biophysics reports · 2026Review
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- Plasma, Urinary, and Salivary Total Redox Status in Critically Ill Patients with Brain Injury and Secondary Organ Failure.Antioxidants (Basel, Switzerland) · 2026Article
- Special Issue "Immune-Inflammatory and Oxidative Stress Signaling Pathways Involved in Human Disorders".International journal of molecular sciences · 2026Article
- Nutritional Modulation of the Gut-Kidney Axis.Nutrients · 2026Review
- Buckling-Resistant and Trace-Stacked (BRATS) Design Enables Aid-Free Implantation of Flexible Multielectrode Array with Minimized Inflammatory Tissue Response.Advanced functional materials · 2026Article
- Insights into the potential pathogenesis and therapeutic implications of ferroptosis in brain microvascular endothelial cells during stroke.Frontiers in immunology · 2026Review
- CSF1R and IL1R1 inhibitors synergistically attenuate the early pathogenesis of traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Exosome-Based Diagnostics and Cell-Free Therapeutics for Traumatic Brain Injury: From Mechanisms to Bedside.International journal of nanomedicine · 2026Review
- Injectable reactive oxygen and nitrogen species-scavenging hydrogels for repairing traumatic brain injury.Materials today. Bio · 2025Article
- Integration of transcriptomics and metabolomics to study the mechanism of Siwei Huangqi powder in Tibetan medicine for protecting against high-altitude hypoxic brain injuries.Journal of traditional and complementary medicine · 2025Article
- Nutritional Modulation of the Endogenous Antioxidant System in the Brain-Gut Axis Following Traumatic Brain Injury.Nutrients · 2025Article
- Recent advances in theranostic nanomaterials for overcoming traumatic brain injury.Journal of nanobiotechnology · 2025Review
- Role of transforming growth factorβ in neurovascular unit during cerebral small vessel disease.Fluids and barriers of the CNS · 2025Review
- Beyond cardiac embolism and cryptogenic stroke: unveiling the mechanisms of cerebrovascular events in Chagas disease.Lancet regional health. Americas · 2025Review
- Influence of traumatic brain injury on serum levels of pituitary, thyroid, adrenal and gonadal hormones.Medicine · 2025Observational
- Evaluating the S100β, GFAP, IL-6, and Oxidative Stress Markers in Traumatic Brain Injury.Cureus · 2025Article
- Stroke-Induced Retinal Dysfunction: Mechanisms, Diagnostics, and Future Directions.Aging and disease · 2025Review
- Temporal Changes in Mitochondria-Centric Excitotoxic Responses Following Severe Penetrating Traumatic Brain Injury.Biomedicines · 2025Article
169 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a major cause of death in the young age group and leads to persisting neurological impairment in many of its victims. It may result in permanent functional deficits because of both primary and secondary damages. This review addresses the role of oxidative stress in TBI-mediated secondary damages by affecting the function of the vascular unit, changes in blood-brain barrier (BBB) permeability, posttraumatic edema formation, and modulation of various pathophysiological factors such as inflammatory factors and enzymes associated with trauma. Oxidative stress plays a major role in many pathophysiologic changes that occur after TBI. In fact, oxidative stress occurs when there is an impairment or inability to balance antioxidant production with reactive oxygen species (ROS) and reactive nitrogen species (RNS) levels. ROS directly downregulate proteins of tight junctions and indirectly activate matrix metalloproteinases (MMPs) that contribute to open the BBB. Loosening of the vasculature and perivascular unit by oxidative stress-induced activation of MMPs and fluid channel aquaporins promotes vascular or cellular fluid edema, enhances leakiness of the BBB, and leads to progression of neuroinflammation. Likewise, oxidative stress activates directly the inflammatory cytokines and growth factors such as IL-1β, tumor necrosis factor-α (TNF-α), and transforming growth factor-beta (TGF-β) or indirectly by activating MMPs. In another pathway, oxidative stress-induced degradation of endothelial vascular endothelial growth factor receptor-2 (VEGFR-2) by MMPs leads to a subsequent elevation of cellular/serum VEGF level. The decrease in VEGFR-2 with a subsequent increase in VEGF-A level leads to apoptosis and neuroinflammation via the activation of caspase-1/3 and IL-1β release.
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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.