ArticleTherapeutic targets for neurological diseases2015
Targeting heme oxygenase after intracerebral hemorrhage.
Article in Therapeutic targets for neurological diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Cinnamaldehyde and its combination with deferoxamine ameliorate inflammation, ferroptosis and hematoma expansion after intracerebral hemorrhage in mice.Journal of neuroinflammation · 2025Article
- Involvement of EGFR-AKT signaling in hemin-induced neurotoxicity.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Review
- Secondary Brain Injury by Oxidative Stress After Cerebral Hemorrhage: Recent Advances.Frontiers in cellular neuroscience · 2022Review
- Research Progress in Understanding the Relationship Between Heme Oxygenase-1 and Intracerebral Hemorrhage.Frontiers in neurology · 2018Review
- Cofilin signaling in hemin-induced microglial activation and inflammation.Journal of neuroimmunology · 2017Article
- Article
- Neuronal Death After Hemorrhagic Stroke In Vitro and In Vivo Shares Features of Ferroptosis and Necroptosis.Stroke · 2017Article
- Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage.Molecular neurobiology · 2017Review
- The role of heme oxygenase-1 (HO-1) in the regulation of inflammatory reaction, neuronal cell proliferation and apoptosis in rats after intracerebral hemorrhage (ICH).Neuropsychiatric disease and treatment · 2017Article
- Distinct role of heme oxygenase-1 in early- and late-stage intracerebral hemorrhage in 12-month-old mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Molecular pathophysiology of cerebral edema.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Review
- Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy.Oxidative medicine and cellular longevity · 2016Review
- Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets.Oxidative medicine and cellular longevity · 2016Review
- Effects of human umbilical cord mesenchymal stem cell transplantation combined with minimally invasive hematoma aspiration on intracerebral hemorrhage in rats.American journal of translational research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Intracerebral hemorrhage (ICH) is the primary event in approximately 10% of strokes, and has higher rates of morbidity and mortality than ischemic stroke. Experimental evidence suggests that the toxicity of hemoglobin and its degradation products contributes to secondary injury that may be amenable to therapeutic intervention. Hemin, the oxidized form of heme, accumulates in intracranial hematomas to cytotoxic levels. The rate limiting step of its breakdown is catalyzed by the heme oxygenase (HO) enzymes, which consist of inducible HO-1 and constitutively-expressed HO-2. The effect of these enzymes on perihematomal injury and neurological outcome has been investigated in ICH models using both genetic and pharmacological approaches to alter their expression, with variable results reported. These findings are summarized and reconciled in this review; therapeutic strategies that may optimize HO expression and activity after ICH are described.
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.