ReviewMolecular neurobiology2020
Blood-Related Toxicity after Traumatic Brain Injury: Potential Targets for Neuroprotection.
Review in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 21 citations in OpenAlex.
- Epigenetic mechanisms in traumatic brain injury: a focus on astrocytes and therapeutic implications.Journal of neuroinflammation · 2026Review
- Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.Inflammopharmacology · 2025Review
- Unraveling the Mystery of Hemoglobin in Hypoxia-Accelerated Neurodegenerative Diseases.Biomolecules · 2025Review
- Deferoxamine Induces Autophagy Following Traumatic Brain Injury via TREM2 on Microglia.Molecular neurobiology · 2024Article
- Article
- Ultrasound imaging guided precision histotripsy: Effects of pulse settings on ablation properties in rat brain.The Journal of the Acoustical Society of America · 2024Article
- Hydrophobic Polystyrene-Modified Gelatin Enhances Fast Hemostasis and Tissue Regeneration in Traumatic Brain Injury.Advanced healthcare materials · 2023Article
- The Haptoglobin Response after Aneurysmal Subarachnoid Haemorrhage.International journal of molecular sciences · 2023Article
- Protective Roles of Hydrogen Sulfide in Alzheimer's Disease and Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2023Review
- Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury.Biomedicines · 2023Review
- Twelve protections evolved for the brain, and their roles in extending its functional life.Frontiers in neuroanatomy · 2023Review
- Protective role of wogonin following traumatic brain injury by reducing oxidative stress and apoptosis via the PI3K/Nrf2/HO‑1 pathway.International journal of molecular medicine · 2022Article
- Inflammation and Oxidative Stress: Potential Targets for Improving Prognosis After Subarachnoid Hemorrhage.Frontiers in cellular neuroscience · 2021Review
- Anti-inflammatory and Neuroprotective Agents in Clinical Trials for CNS Disease and Injury: Where Do We Go From Here?Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Emergency visits, hospitalizations, and deaths due to traumatic brain injury (TBI) have increased significantly over the past few decades. While the primary early brain trauma is highly deleterious to the brain, the secondary injury post-TBI is postulated to significantly impact mortality. The presence of blood, particularly hemoglobin, and its breakdown products and key binding proteins and receptors modulating their clearance may contribute significantly to toxicity. Heme, hemin, and iron, for example, cause membrane lipid peroxidation, generate reactive oxygen species, and sensitize cells to noxious stimuli resulting in edema, cell death, and increased morbidity and mortality. A wide range of other mechanisms such as the immune system play pivotal roles in mediating secondary injury. Effective scavenging of all of these pro-oxidant and pro-inflammatory metabolites as well as controlling maladaptive immune responses is essential for limiting toxicity and secondary injury. Hemoglobin metabolism is mediated by key molecules such as haptoglobin, heme oxygenase, hemopexin, and ferritin. Genetic variability and dysfunction affecting these pathways (e.g., haptoglobin and heme oxygenase expression) have been implicated in the difference in susceptibility of individual patients to toxicity and may be target pathways for potential therapeutic interventions in TBI. Ongoing collaborative efforts are required to decipher the complexities of blood-related toxicity in TBI with an overarching goal of providing effective treatment options to all patients with TBI.
Indexed as
Identifiers
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.