Analysis Tools
homeostasis/metabolism
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• mice exhibit aggravated ventricular remodeling and cardiac dysfunction 28 days post-myocardial infraction (MI), with lower left ventricular ejection fraction and fractional shortening than wild-type mice, larger interstitial fibrosis area and increased markers of fibrosis in the infarcted border zone, and increased recruitment of macrophages to the infarcted border zone
• mice show increased susceptibility to ventricular arrhythmia post-myocardial infarction
• treatment with blockers of p38 and JNK, Losmapimod and SP600125, alleviates the ventricular remodeling in mice 28 days post-MI
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• mice exhibit larger infarct size 28 days post-MI
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• neonatal mouse ventricular cardiomyocytes (NMVMs) under hypoxia conditions show aggravated apoptosis and hypertrophy compared to wild-type NMVMs
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cardiovascular system
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• mice show a larger interstitial fibrosis area and increased markers of fibrosis in the infarcted border zone 28 days post-MI
• mice treated with the selective NLRP3 inflammasome inhibitor MCC950 show reduced cardiac fibrosis that occurs following MI
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• intracardiac programmed electrical stimulation shows that mice present elevated inducibility and duration of ventricular tachycardia/ventricular fibrillation (VT/VF) by burst pacing 28 days post-MI
• mice treated with MCC950 show reduced inducibility and VT/VF duration that occurs following MI
• treatment with blockers of p38 and JNK, Losmapimod and SP600125, alleviates the pacing-induced VT/VF in mice 28 days post-MI
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• mice show increased susceptibility to ventricular arrhythmia post-myocardial infarction
• however, no difference is heart rate is seen regardless of whether myocardial infarction is performed
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• intracardiac programmed electrical stimulation shows that mice present elevated inducibility and duration of ventricular tachycardia/ventricular fibrillation (VT/VF) by burst pacing 28 days post-MI
• mice treated with MCC950 show reduced inducibility and VT/VF duration that occurs following MI
• treatment with blockers of p38 and JNK, Losmapimod and SP600125, alleviates the pacing-induced VT/VF in mice 28 days post-MI
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• mice show many more premature ventricular contraction (PVC) events than controls 28 days post-myocardial infarction
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• mice exhibit aggravated ventricular remodeling and cardiac dysfunction 28 days post-myocardial infraction (MI), with lower left ventricular ejection fraction and fractional shortening than wild-type mice, larger interstitial fibrosis area and increased markers of fibrosis in the infarcted border zone, and increased recruitment of macrophages to the infarcted border zone
• mice show increased susceptibility to ventricular arrhythmia post-myocardial infarction
• treatment with blockers of p38 and JNK, Losmapimod and SP600125, alleviates the ventricular remodeling in mice 28 days post-MI
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• mice exhibit larger infarct size 28 days post-MI
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