ArticleAmerican journal of physiology. Heart and circulatory physiology2020
Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of nonreperfused myocardial infarction.
Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021Guideline
- Short-chain fatty acids promote post-myocardial infarction cardiac repair via FFAR2-dependent suppression of osteoclast-like macrophage differentiation.Basic research in cardiology · 2026Article
- Cardiomyocyte-Specific Smad7 Protects the Pressure-Overloaded Heart, Inhibiting the Transforming Growth Factor-β Receptor 1/Smad2/3 Cascade.Journal of the American Heart Association · 2026Article
- Suppression of CSF2RA macrophage polarisation impacts pathological cardiac remodelling in mice.Scientific reports · 2026Article
- Decoding cardiac homeostasis and injury: the evolving landscape of spatial transcriptomics.Frontiers in cell and developmental biology · 2026Review
- Article
- Cardiomyocyte Alpha-1A Adrenergic Receptors Mitigate Postinfarct Remodeling and Mortality by Constraining Necroptosis.JACC. Basic to translational science · 2024Article
- Protective effects of macrophage-specific integrin α5 in myocardial infarction are associated with accentuated angiogenesis.Nature communications · 2023Article
- Don't go breakin' my heart: cardioprotective alterations to the mechanical and structural properties of reperfused myocardium during post-infarction inflammation.Biophysical reviews · 2023Review
- The cardiac wound healing response to myocardial infarction.WIREs mechanisms of disease · 2023Review
- Unraveling the role of galectin-3 in cardiac pathology and physiology.Frontiers in physiology · 2023Review
- Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022Review
- The role of endogenous Smad7 in regulating macrophage phenotype following myocardial infarction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Smad-dependent pathways in the infarcted and failing heart.Current opinion in pharmacology · 2022Review
- Ensemble machine learning model identifies patients with HFpEF from matrix-related plasma biomarkers.American journal of physiology. Heart and circulatory physiology · 2022Article
- Review
- Macrophages secrete murinoglobulin-1 and galectin-3 to regulate neutrophil degranulation after myocardial infarction.Molecular omics · 2022Article
- Smad7 effects on TGF-β and ErbB2 restrain myofibroblast activation and protect from postinfarction heart failure.The Journal of clinical investigation · 2022Article
- S100A9 is a functional effector of infarct wall thinning after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2022Article
- Neutrophil crosstalk during cardiac wound healing after myocardial infarction.Current opinion in physiology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In patients with myocardial infarction (MI), cardiac rupture is an uncommon but catastrophic complication. In the mouse model of nonreperfused MI, reported rupture rates are highly variable and depend not only on the genetic background and sex of animals but also on the method used for documentation of rupture. In most studies, diagnosis of cardiac rupture is based on visual inspection during autopsy; however, criteria are poorly defined. We performed systematic histopathological analysis of whole hearts from C57BL/6J mice dying after nonreperfused MI and evaluated the reliability of autopsy-based criteria in identification of rupture. Moreover, we compared the cell biological environment of the infarct between rupture-related and rupture-independent deaths. Histopathological analysis documented rupture in 50% of mice dying during the first week post-MI. Identification of a gross rupture site was highly specific but had low sensitivity; in contrast, hemothorax had high sensitivity but low specificity. Mice with rupture had lower myofibroblast infiltration, accentuated macrophage influx, and a trend toward reduced collagen content in the infarct. Male mice had increased mortality and higher incidence of rupture. However, infarct myeloid cells harvested from male and female mice at the peak of the incidence of rupture had comparable inflammatory gene expression. In conclusion, the reliability of autopsy in documentation of rupture in infarcted mice is dependent on the specific criteria used. Macrophage-driven inflammation and reduced activation of collagen-secreting reparative myofibroblasts may be involved in the pathogenesis of post-MI cardiac rupture.
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Registered trials
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