Effects Of Mesenchymal Stem Cell Transplantation Into Infarcted Myocardium On Cardiac Function And Extracellular Matrix In Rats

Myocardial infarction (MI) is a leading cause of mortality and morbidity of cardiovascular disease. Following occlusion of the left anterior descending coronary artery (LAD), the infarcted myocardium undergoes reparative fibrosis and is replaced by scar tissue after gradual resorption of necrotic cells. Left ventricular remodeling involves expansion of the infarcted area, ventricular dilatation and thinning of the ventricular wall. Myocardial fibrosis is a major component of ventricular remodeling after MI. This process is rapidly initiated to maintain structural integrity and to resist rupture of the ventricle wall. On the other hand, the preservation of cardiac function depends on the remodeling of the surviving myocardial tissue. This cardiac remodeling is characterized by hypertrophy of cardiomyocytes and hyperplasia of non-myocytes and also leads to an adverse interstitial fibrosis at non-infarcted remote sites. Myocardial fibrosis enhances myocardial stiffness, promotes the development of arrhythmias and hampers systolic ejection by rendering the myocardium heterogeneous in composition. Since the unwanted fibrosis contributes to the progression of chronic heart failure, this process has been intensively studied over the past years.Although limited proliferation of endogenous myocardial cells in infarcted myocardium has been reported, massive loss of mammalian myocardium cannot be sufficiently regenerated by the remaining myocytes. In addition, surgical and interventional revalscularisation of ischemic myocardium can treat angina, reduce risk of myocardial infarction, and improve function of viable myocardium, but the...