ArticlePloS one2010
Genetically-defined deficiency of mannose-binding lectin is associated with protection after experimental stroke in mice and outcome in human stroke.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 136 citations in OpenAlex.
- Genetic Variation, Magnesium Sulfate Exposure, and Adverse Neurodevelopmental Outcomes Following Preterm Birth.American journal of perinatology · 2018Trial
- Association between endogenous complement inhibitor and myocardial salvage in patients with myocardial infarction.European heart journal. Acute cardiovascular care · 2014Trial
- Impact of mannose-binding lectin deficiency on radiocontrast-induced renal dysfunction: a post-hoc analysis of a multicenter randomized controlled trial.BMC nephrology · 2012Trial
- Metabolome Wide Mendelian Randomization Assessing the Causal Relationship Between Serum Metabolites, Cerebrospinal Metabolites, and Aneurysmal Subarachnoid Hemorrhage.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Traumatic brain injury persistently increases the incidence of both ischemic and hemorrhagic strokes: Potential mechanisms.Progress in neurobiology · 2025Review
- The immunology of stroke and dementia.Immunity · 2025Review
- Detrimental interactions of hypoxia and complement MASP-1 in endothelial cells as a model for atherosclerosis-related diseases.Scientific reports · 2024Article
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
- The central role of peripheral inflammation in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Complement lectin pathway components MBL and MASP-1 promote haemostasis upon vessel injury in a microvascular bleeding model.Frontiers in immunology · 2022Article
- Role of the lectin pathway of complement in hematopoietic stem cell transplantation-associated endothelial injury and thrombotic microangiopathy.Experimental hematology & oncology · 2021Review
- High serum complement component C4 as a unique predictor of unfavorable outcomes in diabetic stroke.Metabolic brain disease · 2021Article
- Molecular Mechanisms of Neuroimmune Crosstalk in the Pathogenesis of Stroke.International journal of molecular sciences · 2021Review
- β2 glycoprotein I participates in phagocytosis of apoptotic neurons and in vascular injury in experimental brain stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021Review
- Neuroimmune crosstalk and evolving pharmacotherapies in neurodegenerative diseases.Immunology · 2021Review
- MASPs at the crossroad between the complement and the coagulation cascades - the case for COVID-19.Genetics and molecular biology · 2021Article
- Pattern Recognition Molecules of Lectin Complement Pathway in Ischemic Stroke.Pharmacogenomics and personalized medicine · 2021Article
- The good, the bad, and the opportunities of the complement system in neurodegenerative disease.Journal of neuroinflammation · 2020Review
- Precision Medicine in Neurology: The Inspirational Paradigm of Complement Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2020Review
22 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
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe complement system is a major effector of innate immunity that has been involved in stroke brain damage. Complement activation occurs through the classical, alternative and lectin pathways. The latter is initiated by mannose-binding lectin (MBL) and MBL-associated serine proteases (MASPs). Here we investigated whether the lectin pathway contributes to stroke outcome in mice and humans. METHODOLOGY/PRINCIPAL
findingsFocal cerebral ischemia/reperfusion in MBL-null mice induced smaller infarctions, better functional outcome, and diminished C3 deposition and neutrophil infiltration than in wild-type mice. Accordingly, reconstitution of MBL-null mice with recombinant human MBL (rhMBL) enhanced brain damage. In order to investigate the clinical relevance of these experimental observations, a study of MBL2 and MASP-2 gene polymorphism rendering the lectin pathway dysfunctional was performed in 135 stroke patients. In logistic regression adjusted for age, gender and initial stroke severity, unfavourable outcome at 3 months was associated with MBL-sufficient genotype (OR 10.85, p = 0.008) and circulating MBL levels (OR 1.29, p = 0.04). Individuals carrying MBL-low genotypes (17.8%) had lower C3, C4, and CRP levels, and the proinflammatory cytokine profile was attenuated versus MBL-sufficient genotypes. CONCLUSIONS/SIGNIFICANCE: In conclusion, genetically defined MBL-deficiency is associated with a better outcome after acute stroke in mice and humans.
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.