ArticleExperimental and clinical cardiology2013
Validation of the vitronectin knockout mouse as a model for studying myocardial infarction: Vitronectin appears to influence left ventricular remodelling following myocardial infarction.
Article in Experimental and clinical cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Proteomics-based biomarkers of plasma exosomes from patients with acute myocardial infarction.PloS one · 2026Article
- Complement or insult: the emerging link between complement cascade deficiencies and pathology of myeloid malignancies.Journal of leukocyte biology · 2024Review
- The Role of Matrix Proteins in Cardiac Pathology.International journal of molecular sciences · 2022Review
- Fluid Shear Stress and Fibroblast Growth Factor-2 Increase Endothelial Cell-Associated Vitronectin.Applied bionics and biomechanics · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVitronectin (VN) is an abundant acute-phase plasma protein that regulates cell adhesion and migration as well as interactions with components of the plasminogen activator/plasmin system, specifically plasminogen activator inhibitor type 1. This system plays a major role in tissue remodelling regulating wound healing after myocardial infarction.
objectivesTo investigate the feasibility of using VN knockout mice (VN(-/-)) to study the role of VN on ventricular remodelling following myocardial infarction.
methodsSpecifically bred VN(-/-) mice and normal wild-type (VN(+/+)) mice underwent coronary artery ligation and were assessed 28 days postligation using echocardiography and morphometric histology.
resultsNo difference was observed between VN(-/-) mice and VN(+/+) mice with respect to gross phenotype, weight, coronary anatomy or echocardiographically measured ejection fraction (56%). Following myocardial infarction, VN(-/-) mice exhibited less ventricular dilation and less impairment in echocardiographic ejection fraction compared with VN(+/+) mice (48% versus 41%; P=0.01). VN(-/-) mice also exhibited smaller infarcts on morphometric analysis.
conclusionsThe results of the present study confirmed the feasibility of using coronary artery ligation in VN knockout mice to investigate the role of VN in post-myocardial infarction remodelling. The absence of VN appears to result in favourable effects on wound healing. These data suggest that this model may offer novel insights into the role of VN in the regulation of myocardial remodelling.
Indexed as
Identifiers
24294037PMC3716488W2100717328What 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.