ReviewJournal of stroke2020
Neuroinflammation after Intracerebral Hemorrhage and Potential Therapeutic Targets.
Review in Journal of stroke, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 276 papers, 6 of them syntheses that pooled it.
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
276 citing papers in PubMed, 6 syntheses or guidelines pooled it, 466 citations in OpenAlex.
- Pooled it
- Mechanisms of exercise-based rehabilitation following intracerebral hemorrhage: insights from preclinical evidence.Frontiers in pharmacology · 2026Pooled it
- Pathological mechanisms and future therapeutic directions of thrombin in intracerebral hemorrhage: a systematic review.Frontiers in pharmacology · 2024Pooled it
- The core of maintaining neuropathic pain: Crosstalk between glial cells and neurons (neural cell crosstalk at spinal cord).Brain and behavior · 2023Pooled it
- Can Artificial Intelligence Be Applied to Diagnose Intracerebral Hemorrhage under the Background of the Fourth Industrial Revolution? A Novel Systemic Review and Meta-Analysis.International journal of clinical practice · 2022Pooled it
- Prognostic Role of the Neutrophil-to-Lymphocyte Ratio in Intracerebral Hemorrhage: A Systematic Review and Meta-Analysis.Frontiers in neuroscience · 2022Pooled it
- Trial
- TIGAR overexpression alleviates intracerebral hemorrhage injury in mice by suppressing ATF4/NOX4/p22phox-mediated oxidative stress and inflammation.Acta pharmacologica Sinica · 2026Article
- Loss of Pericytic Integrin-β1 Exacerbates Blood-Brain Barrier Damage and Hemorrhagic Brain Injury.Stroke · 2026Article
- Lcn2 Promotes Ferroptosis in Intracerebral Hemorrhage by Targeting Keap1 Tyr572 and Restricting Nrf2 Activation.MedComm · 2026Article
- Selective Kv1.3 inhibition promotes M2 microglial polarization, accelerates hematoma resolution, and improves neurological recovery following collagenase-induced spontaneous intracerebral hemorrhage in mice.Veterinary world · 2026Article
- Microglia heterogeneity in vascular dementia pathology.iScience · 2026Review
- Targeting Microglial C5aR1 with PMX205 Attenuates Neuroinflammation and Improves Neurological Recovery After Intracerebral Hemorrhage.Neurochemical research · 2026Article
- Failed resolution of inflammation in intracerebral haemorrhage.Nature reviews. Neurology · 2026Review
- CD147-Conjugated Minocycline Nanomicelles Alleviate Neuroinflammation and Improve Neurological Function Following Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2026Article
- Tumor necrosis factor-α-stimulated gene 6 promotes hematoma clearance after intracerebral hemorrhage in a mouse model.Neural regeneration research · 2026Article
- Eerdun Wurile, a Mongolian medicine, alleviates neuronal damage and improves neurological dysfunction after cerebral hemorrhage by activating the PI3K/AKT signaling pathway.Chinese medicine · 2026Article
- Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Matrine Attenuates Neurological Deficits and Neuroinflammation by Inhibiting the HMGB1/RAGE Axis and Ferroptosis in Intracerebral Hemorrhage Mice.The Kaohsiung journal of medical sciences · 2026Article
- Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026Article
216 more citing papers are in PubMed but not listed here.
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spontaneous intracerebral hemorrhage (ICH) is a catastrophic illness causing significant morbidity and mortality. Despite advances in surgical technique addressing primary brain injury caused by ICH, little progress has been made treating the subsequent inflammatory cascade. Pre-clinical studies have made advancements identifying components of neuroinflammation, including microglia, astrocytes, and T lymphocytes. After cerebral insult, inflammation is initially driven by the M1 microglia, secreting cytokines (e.g., interleukin-1β [IL-1β] and tumor necrosis factor-α) that are involved in the breakdown of the extracellular matrix, cellular integrity, and the blood brain barrier. Additionally, inflammatory factors recruit and induce differentiation of A1 reactive astrocytes and T helper 1 (Th1) cells, which contribute to the secretion of inflammatory cytokines, augmenting M1 polarization and potentiating inflammation. Within 7 days of ICH ictus, the M1 phenotype coverts to a M2 phenotype, key for hematoma removal, tissue healing, and overall resolution of inflammation. The secretion of anti-inflammatory cytokines (e.g., IL-4, IL-10) can drive Th2 cell differentiation. M2 polarization is maintained by the secretion of additional anti-inflammatory cytokines by the Th2 cells, suppressing M1 and Th1 phenotypes. Elucidating the timing and trigger of the anti-inflammatory phenotype may be integral in improving clinical outcomes. A challenge in current translational research is the absence of an equivalent disease animal model mirroring the patient population and comorbid pathophysiologic state. We review existing data and describe potential therapeutic targets around which we are creating a bench to bedside translational research model that better reflects the pathophysiology of ICH patients.
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.