ArticleLaboratory investigation; a journal of technical methods and pathology2019
Phenotypic characterization of murine models of cerebral cavernous malformations.
Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 26 citations in OpenAlex.
- CXCL13⁺ CD4⁺ T cells are associated with B-cell recruitment and lesion progression in cerebral cavernous malformations.Journal of neuroinflammation · 2026Article
- Familial Cerebral Cavernous Malformations: Pathophysiology, Genetics, Biomarkers, and Treatment Perspectives.Journal of neurochemistry · 2026Review
- Pathologic features of brain hemorrhage after radiation treatment: case series with somatic mutation analysis.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2024Article
- Tailored management of cavernous malformations in women: considerations and strategies-a review.Frontiers in neurology · 2024Review
- Circulating Plasma miRNA Homologs in Mice and Humans Reflect Familial Cerebral Cavernous Malformation Disease.Translational stroke research · 2023Article
- Clinicoradiologic data of familial cerebral cavernous malformation with age-related disease burden.Annals of clinical and translational neurology · 2023Article
- Heterozygous Loss of KRIT1 in Mice Affects Metabolic Functions of the Liver, Promoting Hepatic Oxidative and Glycative Stress.International journal of molecular sciences · 2022Article
- Contact-dependent signaling triggers tumor-like proliferation of CCM3 knockout endothelial cells in co-culture with wild-type cells.Cellular and molecular life sciences : CMLS · 2022Article
- Cerebral Cavernous Malformation Pathogenesis: Investigating Lesion Formation and Progression with Animal Models.International journal of molecular sciences · 2022Review
- Inflammation and neutrophil extracellular traps in cerebral cavernous malformation.Cellular and molecular life sciences : CMLS · 2022Article
- The multifacetedGenes & diseases · 2021Review
- Bringing CCM into a dish: cell culture models for cerebral cavernous malformations.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2021Article
- Cerebral Cavernous Malformation: From Mechanism to Therapy.Circulation research · 2021Review
- Article
- Novel Murine Models of Cerebral Cavernous Malformations.Angiogenesis · 2020Article
- Common transcriptome, plasma molecules, and imaging signatures in the aging brain and a Mendelian neurovascular disease, cerebral cavernous malformation.GeroScience · 2020Article
- Antibodies in cerebral cavernous malformations react with cytoskeleton autoantigens in the lesional milieu.Journal of autoimmunity · 2020Observational
- Distinct cellular roles for PDCD10 define a gut-brain axis in cerebral cavernous malformation.Science translational medicine · 2019Article
- Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations.Acta neuropathologica communications · 2019Article
- Cavernous angiomas: deconstructing a neurosurgical disease.Journal of neurosurgery · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 4 institutions in 1 country.
Funding
Abstract
Cerebral cavernous malformations (CCMs) are clusters of dilated capillaries that affect around 0.5% of the population. CCMs exist in two forms, sporadic and familial. Mutations in three documented genes, KRIT1(CCM1), CCM2, and PDCD10(CCM3), cause the autosomal dominant form of the disease, and somatic mutations in these same genes underlie lesion development in the brain. Murine models with constitutive or induced loss of respective genes have been applied to study disease pathobiology and therapeutic manipulations. We aimed to analyze the phenotypic characteristic of two main groups of models, the chronic heterozygous models with sensitizers promoting genetic instability, and the acute neonatal induced homozygous knockout model. Acute model mice harbored a higher lesion burden than chronic models, more localized in the hindbrain, and largely lacking iron deposition and inflammatory cell infiltrate. The chronic model mice showed a lower lesion burden localized throughout the brain, with significantly greater perilesional iron deposition, immune B- and T-cell infiltration, and less frequent junctional protein immunopositive endothelial cells. Lesional endothelial cells in both models expressed similar phosphorylated myosin light chain immunopositivity indicating Rho-associated protein kinase activity. These data suggest that acute models are better suited to study the initial formation of the lesion, while the chronic models better reflect lesion maturation, hemorrhage, and inflammatory response, relevant pathobiologic features of the human disease.
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.