Abstract
The adult mammalian heart has negligible regenerative capacity; thus, repair of the infarcted myocardium requires formation of a collagen-based scar. As the infarct heals, the ventricle remodels undergoing dilation and exhibiting progressive dysfunction. In patients with myocardial infarction, dilative remodeling is an adverse prognostic indicator, associated with mortality, arrhythmias, and a high incidence of heart failure. The severity of adverse remodeling is not dependent only on the size of the acute infarct, but is also greatly affected by the qualitative characteristics of the reparative response. Extensive experimental evidence suggests that effective repair of the infarcted heart requires timely induction and suppression of inflammatory cytokines and growth factors, resulting in sequential activation, mobilization and de-activation of immune cells, vascular cells and fibroblasts [ [1] Latet S.C. Hoymans V.Y. Van Herck P.L. Vrints C.J. The cellular immune system in the post-myocardial infarction repair process. Int. J. Cardiol. 2015; 179: 240-247 Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar , [2] Frangogiannis N.G. The inflammatory response in myocardial injury, repair, and remodelling. Nat. Rev. Cardiol. 2014; 11: 255-265 Crossref PubMed Scopus (747) Google Scholar ]. Platelet derived growth factor-A (Pdgf-a) gene transfer modulates scar composition and improves left ventricular function after myocardial infarctionInternational Journal of CardiologyVol. 341PreviewBackground: Novel therapies that can limit or reverse damage caused by myocardial infarction (MI) could ease the increasing burden of heart failure. In this regard Platelet Derived Growth Factor (PDGF) has been previously shown to contribute to cardiac repair after MI. Here, we use a rodent model of MI and recombinant adeno-associated virus 9 (rAAV9)-mediated gene transfer to overexpress Pdgf-a in the injured heart and assess its therapeutic potential.Methods and results: Sprague Dawley rats underwent temporary occlusion of the left anterior descending coronary artery, followed immediately by systemic delivery of 1 × 10^11 vector genomes of either rAAV9 Pdgf-a or rAAV9 Empty vector (control). Full-Text PDF
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