ReviewFrontiers in immunology2019
Therapeutic Modulation of the Complement Cascade in Stroke.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis 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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Progressive microvascular failure in acute ischemic stroke: A systematic review, meta-analysis, and time-course analysis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Pooled it
- THE MICROANATOMY OF INTRACRANIAL HUMAN THROMBI BY SINGLE NUCLEI TRANSCRIPTOMICS.bioRxiv : the preprint server for biology · 2026Article
- Review
- Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia-Reperfusion Injury: From Inflammatory Response to Neurorepair.International journal of molecular sciences · 2025Review
- Article
- Article
- Circulating Blood Prognostic Biomarker Signatures for Hemorrhagic Cerebral Cavernous Malformations (CCMs).International journal of molecular sciences · 2024Article
- PolySialic Acid Nanoparticles Actuate Complement-Factor-H-Mediated Inhibition of the Alternative Complement Pathway: A Safer Potential Therapy for Age-Related Macular Degeneration.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Identification and characterization of extrachromosomal circular DNA in large-artery atherosclerotic stroke.Journal of cellular and molecular medicine · 2024Article
- Soluble Biomarkers of Cerebrovascular Pathologies.Stroke · 2024Review
- Human Glial Cells as Innovative Targets for the Therapy of Central Nervous System Pathologies.Cells · 2024Review
- Myeloid CellJournal of inflammation research · 2024Article
- NPD1 Plus RvD1 Mediated Ischemic Stroke Penumbra Protection Increases Expression of Pro-homeostatic Microglial and Astrocyte Genes.Cellular and molecular neurobiology · 2023Article
- Plasma Inflammatory Biomarkers Are Associated With Poststroke Cognitive Impairment: The Nor-COAST Study.Stroke · 2023Observational
- Free complement and complement containing extracellular vesicles as potential biomarkers for neuroinflammatory and neurodegenerative disorders.Frontiers in immunology · 2022Review
- Exogenous inter-α inhibitor proteins prevent cell death and improve ischemic stroke outcomes in mice.The Journal of clinical investigation · 2021Article
- The good, the bad, and the opportunities of the complement system in neurodegenerative disease.Journal of neuroinflammation · 2020Review
- Post-Traumatic Sepsis Is Associated with Increased C5a and Decreased TAFI Levels.Journal of clinical medicine · 2020Article
- Tissue-Type Plasminogen Activator and Tenecteplase-Mediated Increase in Blood Brain Barrier Permeability Involves Cell Intrinsic Complement.Frontiers in neurology · 2020Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke is a leading cause of death and disability worldwide and an increasing number of ischemic stroke patients are undergoing pharmacological and mechanical reperfusion. Both human and experimental models of reperfused ischemic stroke have implicated the complement cascade in secondary tissue injury. Most data point to the lectin and alternative pathways as key to activation, and C3a and C5a binding of their receptors as critical effectors of injury. During periods of thrombolysis use to treat stroke, acute experimental complement cascade blockade has been found to rescue tissue and improves functional outcome. Blockade of the complement cascade during the period of tissue reorganization, repair, and recovery is by contrast not helpful and in fact is likely to be deleterious with emerging data suggesting downstream upregulation of the cascade might even facilitate recovery. Successful clinical translation will require the right clinical setting and pharmacologic strategies that are capable of targeting the key effectors early while not inhibiting delayed repair. Early reports in a variety of disease states suggest that such pharmacologic strategies appear to have a favorable risk profile and offer substantial hope for patients.
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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.