ArticleTranslational stroke research2016
Re-exploring Tumor Necrosis Factor Alpha as a Target for Therapy in Intracerebral Hemorrhage.
Article in Translational stroke research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- miR-221 activates Sox11 to reduce brain injury after intracerebral hemorrhage via inhibiting neuroinflammation.Scientific reports · 2025Article
- Prediction of the outcome of intracerebral hemorrhage by blood neutrophil to lymphocyte ratio: a prospective observational study.Annals of medicine and surgery (2012) · 2024Article
- Article
- Hematoma expansion in intracerebral hemorrhage - the right target?Neurological research and practice · 2023Review
- BCL-3 Promotes Intracerebral Hemorrhage Progression by Increasing Blood-Brain Barrier Permeability, Inflammation, and Cell Apoptosis via Endoplasmic Reticulum Stress.Mediators of inflammation · 2023Article
- Granulocyte colony-stimulating factor protected against brain injury in a rat cerebral hemorrhage model by modulating inflammation.Experimental animals · 2022Article
- Neurovascular Units and Neural-Glia Networks in Intracerebral Hemorrhage: from Mechanisms to Translation.Translational stroke research · 2021Review
- Activated Microglia Exosomes Mediated miR-383-3p Promotes Neuronal Necroptosis Through Inhibiting ATF4 Expression in Intracerebral Hemorrhage.Neurochemical research · 2021Article
- Early Predictors of the Increase in Perihematomal Edema Volume After Intracerebral Hemorrhage: A Retrospective Analysis From the Risa-MIS-ICH Study.Frontiers in neurology · 2021Article
- Exploration of MST1-Mediated Secondary Brain Injury Induced by Intracerebral Hemorrhage in Rats via Hippo Signaling Pathway.Translational stroke research · 2019Article
- The role and therapeutic potential of heat shock proteins in haemorrhagic stroke.Journal of cellular and molecular medicine · 2019Review
- Leukemia Inhibitory Factor Decreases Neurogenesis and Angiogenesis in a Rat Model of Intracerebral Hemorrhage.Current medical science · 2019Article
- Pathophysiological Mechanisms and Potential Therapeutic Targets in Intracerebral Hemorrhage.Frontiers in pharmacology · 2019Review
- NLRP3 Inflammasome in the Pathophysiology of Hemorrhagic Stroke: A Review.Current neuropharmacology · 2019Review
- Neutrophil-to-Lymphocyte Ratio Is an Independent Predictor of 30-Day Mortality of Intracerebral Hemorrhage Patients: a Validation Cohort Study.Neurotoxicity research · 2018Article
- An Update On Medical Treatment for Intracerebral Hemorrhage.Translational stroke research · 2018Article
- Recombinant Netrin-1 binding UNC5B receptor attenuates neuroinflammation and brain injury via PPARγ/NFκB signaling pathway after subarachnoid hemorrhage in rats.Brain, behavior, and immunity · 2018Article
- Melatonin Alleviates Intracerebral Hemorrhage-Induced Secondary Brain Injury in Rats via Suppressing Apoptosis, Inflammation, Oxidative Stress, DNA Damage, and Mitochondria Injury.Translational stroke research · 2018Article
- PERK Pathway Activation Promotes Intracerebral Hemorrhage Induced Secondary Brain Injury by Inducing Neuronal Apoptosis BothFrontiers in neuroscience · 2018Article
- Simvastatin Reduces Neutrophils Infiltration Into Brain Parenchyma After Intracerebral Hemorrhage via Regulating Peripheral Neutrophils Apoptosis.Frontiers in neuroscience · 2018Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage (ICH) is a perplexing condition with high mortality and no treatment beyond supportive care. A major portion of the injurious process is takes place during the hours following the development of hematoma. This so-called secondary injury is characterized by an inflammatory cascade that involves a variety of cytokines, including tumor necrosis factor (TNF)-α. Several studies in the rodent model of ICH have shown a rapid increase in brain concentrations of TNF-α following hematoma induction. There is a reasonable body of evidence from experimental models of ICH suggesting that upregulation of TNF-α adjacent to the hematoma is associated with increased peri-hematomal edema, and that inhibition of TNF-α attenuates the formation and progression of this edema and ultimately improves outcomes. Unfortunately, efforts to expand upon these findings have interminably stalled at the pre-clinical phase. A robust clinical study to validate serum TNF-α as a marker for secondary injury in ICH patients is yet to materialize.
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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.