scholarly journals Peroxisome proliferator activated-receptor agonism and left ventricular remodeling in mice with chronic myocardial infarction

2004 ◽  
Vol 141 (1) ◽  
pp. 9-14 ◽  
Author(s):  
Stefan Frantz ◽  
Kai Hu ◽  
Julian Widder ◽  
Barbara Bayer ◽  
Catharina Clara Witzel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Peroxisome Proliferator ◽  
Chronic Myocardial Infarction ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals Effect of Cardiac Stem Cells on Left-Ventricular Remodeling in a Canine Model of Chronic Myocardial Infarction

2013 ◽  
Vol 6 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Frederick G.P. Welt ◽  
Robert Gallegos ◽  
John Connell ◽  
Jan Kajstura ◽  
Domenico D’Amario ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Canine Model ◽  
Left Ventricular ◽  
Cardiac Stem Cells ◽  
Chronic Myocardial Infarction

scholarly journals Injectable Myocardial Matrix Hydrogel Mitigates Negative Left Ventricular Remodeling in a Chronic Myocardial Infarction Model

2020 ◽  
Author(s):  
Miranda D. Diaz ◽  
Elaine Tran ◽  
Jean W. Wassenaar ◽  
Martin Spang ◽  
Roberto Gaetani ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Small Animal ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Chronic Myocardial Infarction ◽  
Decellularized Extracellular Matrix ◽  
The Matrix ◽  
Magnetic Resonance Imaging Mri

SummaryA first-in-man clinical study on a myocardial-derived decellularized extracellular matrix (ECM) hydrogel yielded evidence for potential efficacy in ischemic heart failure (HF) patients. However, little is understood about the mechanism of action in chronic myocardial infarction (MI). In this study we investigated efficacy and mechanism by which the myocardial matrix hydrogel can mitigate negative left ventricular (LV) remodeling in a chronic model of MI. Assessment of cardiac function via magnetic resonance imaging (MRI) demonstrated preservation of LV volumes and apical wall thickening. Differential gene expression analyses showed the matrix is able to prevent worsening HF in a small animal chronic MI model through modulation of the immune response, downregulation of pathways involved in HF progression and fibrosis, and upregulation of genes important for cardiac muscle contraction.

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