ReviewCurrent pharmaceutical design2017
Targeting the Nrf2-Heme Oxygenase-1 Axis after Intracerebral Hemorrhage.
Review in Current pharmaceutical design, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 61 citations in OpenAlex.
- Plant-Derived Natural Compounds and Nrf2-Centered Redox Signaling in Intracerebral Hemorrhage: Evidence Grading, Mechanistic Boundaries, and Translational Challenges.Antioxidants (Basel, Switzerland) · 2026Review
- Lycopene Attenuates Hexavalent Chromium-Induced Hepatotoxicity in Mice by Modulating the Nrf2 Signaling Pathway and the Unfolded Protein Response.Biological trace element research · 2026Article
- Neuroprotection From Intracerebral Hemorrhage Following Pharmacological Inhibition of GSK3β Depends on HFE Gene Status.Journal of neurochemistry · 2026Article
- Neuron-Derived Sema3B Facilitates Microglial Hematoma Clearance After Intracerebral Hemorrhage.Antioxidants (Basel, Switzerland) · 2026Article
- Neuroprotective effects of SRS11-92 against oxidative stress-induced senescence via Nrf2/HO-1/NF-κB in Alzheimer's disease models.Inflammopharmacology · 2026Article
- Dimethyl Fumarate Attenuates Behavioral and Structural Impairments Associated with Brain Ischemia in Rats.Central nervous system agents in medicinal chemistry · 2026Article
- Hemin-induced transient senescence via DNA damage response: a neuroprotective mechanism against ferroptosis in intracerebral hemorrhage.Communications biology · 2025Article
- Mechanism of heme oxygenase-1 regulation of ferroptosis in vascular dementia.Frontiers in molecular neuroscience · 2025Review
- Dose-Dependent Modulation of NMDA Receptors: Neuroprotective Mechanisms against Oxidative Stress in Hippocampal Neurons.International journal of molecular and cellular medicine · 2025Article
- MiRNAs as potential therapeutic targets and biomarkers for non-traumatic intracerebral hemorrhage.Biomarker research · 2024Review
- Common Mutation in theStroke · 2023Article
- Srs11-92, a ferrostatin-1 analog, improves oxidative stress and neuroinflammation via Nrf2 signal following cerebral ischemia/reperfusion injury.CNS neuroscience & therapeutics · 2023Article
- An enriched environment improves long-term functional outcomes in mice after intracerebral hemorrhage by mechanisms that involve the Nrf2/BDNF/glutaminase pathway.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Immunological dimensions of neuroinflammation and microglial activation: exploring innovative immunomodulatory approaches to mitigate neuroinflammatory progression.Frontiers in immunology · 2023Review
- Zhilong Huoxue Tongyu capsule attenuates intracerebral hemorrhage induced redox imbalance by modulation of Nrf2 signaling pathway.Frontiers in pharmacology · 2023Article
- Dimethyl Fumarate Triggers the Antioxidant Defense System in Human Retinal Endothelial Cells through Nrf2 Activation.Antioxidants (Basel, Switzerland) · 2022Article
- Targeting Oxidative Stress in Intracerebral Hemorrhage: Prospects of the Natural Products Approach.Antioxidants (Basel, Switzerland) · 2022Review
- Antioxidant potential of Pediococcus pentosaceus strains from the sow milk bacterial collection in weaned piglets.Microbiome · 2022Article
- Crocin Alleviates Intracerebral Hemorrhage-Induced Neuronal Ferroptosis by Facilitating Nrf2 Nuclear Translocation.Neurotoxicity research · 2022Article
- Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets.Frontiers in immunology · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInjury to cells adjacent to an intracerebral hemorrhage (ICH) is likely mediated at least in part by toxins released from the hematoma that initiate complex and interacting injury cascades. Pharmacotherapies targeting a single toxin or pathway, even if consistently effective in controlled experimental models, have a high likelihood of failure in a variable clinical setting. Nuclear factor erythroid-2 related factor 2 (Nrf2) regulates the expression of heme oxygenase-1 (HO-1) and multiple other proteins with antioxidant and antiinflammatory effects, and may be a target of interest after ICH.
methodsStudies that tested the effect of HO and Nrf2 in models relevant to ICH are summarized, with an effort to reconcile conflicting data by consideration of methodological limitations.
resultsIn vitro studies demonstrated that Nrf2 activators rapidly increased HO-1 expression in astrocytes, and reduced their vulnerability to hemoglobin or hemin. Modulating HO-1 expression via genetic approaches yielded similar results. Systemic treatment with small molecule Nrf2 activators increased HO-1 expression in perivascular cells, particularly astrocytes. When tested in mouse or rat ICH models, Nrf2 activators were consistently protective, improving barrier function and attenuating edema, inflammation, neuronal loss and neurological deficits. These effects were mimicked by selective astrocyte HO-1 overexpression in transgenic mice.
conclusionSystemic treatment with Nrf2 activators after ICH is protective in rodents. Two compounds, dimethyl fumarate and hemin, are currently approved for treatment of multiple sclerosis and acute porphyria, respectively, and have acceptable safety profiles over years of clinical use. Further development of these drugs as ICH therapeutics seems warranted.
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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.