ArticleCirculation2006
Factor XIII deficiency causes cardiac rupture, impairs wound healing, and aggravates cardiac remodeling in mice with myocardial infarction.
Article in Circulation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 167 citations in OpenAlex.
- Human adult and pediatric multimodal transcriptomic atlas of progression from pressure-loaded to failing right ventricle.Nature cardiovascular research · 2026Article
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Molecular Imaging of Collagen Turnover in Myocardial Infarction.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026Article
- Human Transglutaminases: Updated Insights into Activation Mechanisms, Allosteric Regulation and Disease.International journal of molecular sciences · 2026Review
- Molecular Imaging of Collagen Turnover in Myocardial Infarction.bioRxiv : the preprint server for biology · 2026Article
- Linking factor XIII activity to all-cause mortality after myocardial infarction: the overlooked role of serum albumin.International journal of cardiology. Heart & vasculature · 2025Article
- Temporal dynamics of the multi-omic response reveals the modulation of macrophage subsets post-myocardial infarction.Journal of translational medicine · 2025Article
- Plasma Exosomal Proteomics Identifies Differentially Expressed Proteins as Biomarkers for Acute Myocardial Infarction.Biomolecules · 2025Article
- Differential Role of Factor XIII in Acute Myocardial Infarction and Ischemic Stroke.Biomedicines · 2024Review
- Recent advances in positron emission tomography for detecting early fibrosis after myocardial infarction.Frontiers in cardiovascular medicine · 2024Review
- miRNAs Epigenetic Tuning of Wall Remodeling in the Early Phase after Myocardial Infarction: A Novel Epidrug Approach.International journal of molecular sciences · 2023Review
- Fbg αC 389-402 Enhances Factor XIII Cross-Linking in the Fibrinogen αC Region Via Electrostatic and Hydrophobic Interactions.Biochemistry · 2023Article
- Expression of factor XIII originating from synovial fibroblasts and macrophages induced by interleukin-6 signaling.Inflammation and regeneration · 2023Article
- Monocytes Expose Factor XIII-A and Stabilize Thrombi against Fibrinolytic Degradation.International journal of molecular sciences · 2021Article
- Transglutaminases Are Active in Perivascular Adipose Tissue.International journal of molecular sciences · 2021Article
- Factor XIII-A in Diseases: Role Beyond Blood Coagulation.International journal of molecular sciences · 2021Review
- Transglutaminase 2 moderates the expansion of mouse abdominal aortic aneurysms.JVS-vascular science · 2021Article
- Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of nonreperfused myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2020Article
- Coagulation factor XIII activity predicts left ventricular remodelling after acute myocardial infarction.ESC heart failure · 2020Article
- Factor XIIIa inhibitors as potential novel drugs for venous thromboembolism.European journal of medicinal chemistry · 2020Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundIdentification of key molecular players in myocardial healing could lead to improved therapies, reduction of scar formation, and heart failure after myocardial infarction (MI). We hypothesized that clotting factor XIII (FXIII), a transglutaminase involved in wound healing, may play an important role in MI given prior clinical and mouse model data. METHODS AND
resultsTo determine whether a truly causative relationship existed between FXIII activity and myocardial healing, we prospectively studied myocardial repair in FXIII-deficient mice. All FXIII(-/-) and FXIII(-)(/+) (FXIII activity <5% and 70%) mice died within 5 days after MI from left ventricular rupture. In contradistinction, FXIII(-/-) mice that received 5 days of intravenous FXIII replacement therapy had normal survival rates; however, cardiac MRI demonstrated worse left ventricular remodeling in these reconstituted FXIII(-/-) mice. Using a FXIII-sensitive molecular imaging agent, we found significantly greater FXIII activity in wild-type mice and FXIII(-/-) mice receiving supplemental FXIII than in FXIII(-/-) mice (P<0.05). In FXIII(-/-) but not in reconstituted FXIII(-/-) mice, histology revealed diminished neutrophil migration into the MI. Reverse transcriptase-polymerase chain reaction studies suggested that the impaired inflammatory response in FXIII(-/-) mice was independent of intercellular adhesion molecule and lipopolysaccharide-induced CXC chemokine, both important for cell migration. After MI, expression of matrix metalloproteinase-9 was 650% higher and collagen-1 was 53% lower in FXIII(-/-) mice, establishing an imbalance in extracellular matrix turnover and providing a possible mechanism for the observed cardiac rupture in the FXIII(-/-) mice.
conclusionsThese data suggest that FXIII has an important role in murine myocardial healing after infarction.
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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.