ReviewHistology and histopathology2020
Mechanisms of neuroinflammation and inflammatory mediators involved in brain injury following subarachnoid hemorrhage.
Review in Histology and histopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 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
28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.
- Calpain Inhibitors as Potential Therapeutic Modulators in Neurodegenerative Diseases.Neurochemical research · 2022Pooled it
- Lessons Learned from Phase II and Phase III Trials Investigating Therapeutic Agents for Cerebral Ischemia Associated with Aneurysmal Subarachnoid Hemorrhage.Neurocritical care · 2022Pooled it
- Possible Impact of Lymphatic Drainage on Brain Injury After Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2026Review
- Hirudin Alleviates Early Brain Injury After Subarachnoid Hemorrhage in Rats via Regulating NLRP3 Inflammasome-Mediated Pyroptosis.Physiological research · 2025Article
- Tenascin-C as a Target for Intervention in Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.Acta neurochirurgica. Supplement · 2025Review
- Targeting the P2X7 receptor in cerebrovascular diseases: from molecular mechanisms to preclinical therapeutic potential.Frontiers in pharmacology · 2025Review
- The correlation between inflammatory markers and postoperative pulmonary infection in patients with aneurysmal subarachnoid hemorrhage and the construction of prediction model.Frontiers in neurology · 2025Article
- Sirtuins as Potential Targets for Neuroprotection: Mechanisms of Early Brain Injury Induced by Subarachnoid Hemorrhage.Translational stroke research · 2024Review
- Enhancing Th17 cells drainage through meningeal lymphatic vessels alleviate neuroinflammation after subarachnoid hemorrhage.Journal of neuroinflammation · 2024Article
- Anti-Apoptotic Effects of AMPA Receptor Antagonist Perampanel in Early Brain Injury After Subarachnoid Hemorrhage in Mice.Translational stroke research · 2024Article
- SIRT2 Promotes NLRP3-Mediated Microglia Pyroptosis and Neuroinflammation via FOXO3a Pathway After Subarachnoid Hemorrhage.Journal of inflammation research · 2024Article
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
- Effects of New-Generation Antiepileptic Drug Prophylaxis on Delayed Neurovascular Events After Aneurysmal Subarachnoid Hemorrhage.Translational stroke research · 2023Article
- Plasma SPARC Elevation in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- New Insights of Early Brain Injury after Subarachnoid Hemorrhage: A Focus on the Caspase Family.Current neuropharmacology · 2023Article
- Roles of glutamate in brain injuries after subarachnoid hemorrhage.Histology and histopathology · 2022Review
- Neuroelectric Mechanisms of Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2022Review
- Elevated MFG-E8 in CSF in the Early Stage Indicates Rapid Recovery of Mild Aneurysmal SAH Patients.Disease markers · 2022Article
- Melatonin as a Potential Neuroprotectant: Mechanisms in Subarachnoid Hemorrhage-Induced Early Brain Injury.Frontiers in aging neuroscience · 2022Review
- Aneurysmal Subarachnoid Hemorrhage: Review of the Pathophysiology and Management Strategies.Current neurology and neuroscience reports · 2021Review
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 2 countries.
Funding
Abstract
Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disorder. Neuroinflammation is a critical cause of brain injury following SAH in both acute and chronic phases. While accumulating evidence has shown that therapies targeting neuroinflammation exerted beneficial effects in experimental SAH, there is little clinical evidence. One of the factors making neuroinflammation complicated is that inflammatory signaling pathways and mediators act as protective or detrimental responses at different phases. In addition, biomarkers to detect neuroinflammation are little known in clinical settings. In this review, first, we discuss how the inflammatory signaling pathways contribute to brain injury and other secondary pathophysiological changes in SAH. Damage-associated molecular patterns arising from mechanical stress, transient global cerebral ischemia, red blood cell breakdown and delayed cerebral ischemia following SAH trigger to activate pattern recognition receptors (PRRs) such as Toll-like receptors, nucleotide-binding oligomerization domain-like receptors, and receptors for advanced glycation end products. Most of PRRs activate common downstream signaling transcriptional factor nuclear factor-κΒ and mitogen-activated protein kinases, releasing pro-inflammatory mediators and cytokines. Next, we focus on how pro-inflammatory substances play a role during the course of SAH. Finally, we highlight an important inducer of neuroinflammation, matricellular protein (MCP). MCPs are a component of extracellular matrix and exert beneficial and harmful effects through binding to receptors, other matrix proteins, growth factors, and cytokines. Treatment targeting MCPs is being proved efficacious in pre-clinical models for preventing brain injury including neuroinflammation in SAH. In addition, MCPs may be a candidate of biomarkers predicting brain injury following SAH in clinical settings.
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.