ArticleScientific reports2020
Effects on cardiac function, remodeling and inflammation following myocardial ischemia-reperfusion injury or unreperfused myocardial infarction in hypercholesterolemic APOE*3-Leiden mice.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Acteoside attenuates myocardial ischemia reperfusion injury by inhibiting the NLRP3 inflammasome activity via the PI3K/Akt signaling pathway.Scientific reports · 2026Article
- Article
- Age- and sex-specific differences in myocardial sympathetic tone and left ventricular remodeling following myocardial injury.Biology of sex differences · 2025Article
- Restoration of Sestrin 3 Expression Mitigates Cardiac Oxidative Damage in Ischemia-Reperfusion Injury Model.Antioxidants (Basel, Switzerland) · 2025Article
- Detection, Isolation and Quantification of Myocardial Infarct with Four Different Histological Staining Techniques.Diagnostics (Basel, Switzerland) · 2024Article
- Detection, Isolation and Quantification of Myocardial Infarct with Four Different Histological Staining Techniques.bioRxiv : the preprint server for biology · 2024Article
- Cardioprotective effects of Schisantherin A against isoproterenol-induced acute myocardial infarction through amelioration of oxidative stress and inflammation via modulation of PI3K-AKT/Nrf2/ARE and TLR4/MAPK/NF-κB pathways in rats.BMC complementary medicine and therapies · 2023Article
- Multiparametric Immunoimaging Maps Inflammatory Signatures in Murine Myocardial Infarction Models.JACC. Basic to translational science · 2023Article
- Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction.International journal of molecular sciences · 2022Review
- Sclerostin aggravates cardiac remodeling after myocardial infarction by inhibition of Wnt/β-catenin signaling pathway.Journal of thoracic disease · 2022Article
- Effects of swimming training on myocardial protection in rats.Biomedical reports · 2022Article
- Phosphorylcholine antibodies restrict infarct size and left ventricular remodelling by attenuating the unreperfused post-ischaemic inflammatory response.Journal of cellular and molecular medicine · 2021Article
- Expedient assessment of post-infarct remodeling by native cardiac magnetic resonance imaging in mice.Scientific reports · 2021Article
- The Prominin-1-Derived Peptide Improves Cardiac Function Following Ischemia.International journal of molecular sciences · 2021Article
- Post-ischemic Myocardial Inflammatory Response: A Complex and Dynamic Process Susceptible to Immunomodulatory Therapies.Frontiers in cardiovascular medicine · 2021Review
- Toll-Like Receptor 4 Activation Prevents Rat Cardiac Fibroblast Death Induced by Simulated Ischemia/Reperfusion.Frontiers in cardiovascular medicine · 2021Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many novel therapies to treat myocardial infarction (MI), yielding promising results in animal models, nowadays failed in clinical trials for several reasons. The most used animal MI model is based on permanent ligation of the left anterior descending (LAD) coronary artery in healthy mice resulting in transmural MI, while in clinical practice reperfusion is usually accomplished by primary percutaneous coronary interventions (PCI) limiting myocardial damage and inducing myocardial ischemia-reperfusion (MI-R) injury. To evaluate a more similar murine MI model we compared MI-R injury to unreperfused MI in hypercholesterolemic apolipoprotein (APO)E*3-Leiden mice regarding effects on cardiac function, left ventricular (LV) remodeling and inflammation. Both MI-R and MI resulted in significant LV dilation and impaired cardiac function after 3 weeks. Although LV dilation, displayed by end-diastolic (EDV) and end-systolic volumes (ESV), and infarct size (IS) were restricted following MI-R compared to MI (respectively by 27.6% for EDV, 39.5% ESV, 36.0% IS), cardiac function was not preserved. LV-wall thinning was limited with non-transmural LV fibrosis in the MI-R group (66.7%). Two days after inducing myocardial ischemia, local leucocyte infiltration in the infarct area was decreased following MI-R compared to MI (36.6%), whereas systemic circulating monocytes were increased in both groups compared to sham (130.0% following MI-R and 120.0% after MI). Both MI-R and MI models against the background of a hypercholesterolemic phenotype appear validated experimental models, however reduced infarct size, restricted LV remodeling as well as a different distributed inflammatory response following MI-R resemble the contemporary clinical outcome regarding primary PCI more accurately which potentially provides better predictive value of experimental therapies in successive clinical trials.
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