Key result
Coinjection of AAV vectors expressing VEGF and Ang1 improved cardiac perfusion and function in a porcine myocardial infarction model by inducing angiogenesis and reducing apoptosis.
Why the study?
Does coexpression of VEGF and Ang1 improve cardiac function and perfusion in a porcine model of myocardial infarction?
Population
Porcine model of myocardial infarction (MI) induced by ligating the left descending coronary artery
Comparison
Coinjection of Adeno-associated viral vectors… vs Identical dose of AAV-CMVLacZ or saline
Design
Preclinical
Follow-up
8 weeks
Authors
Loading...
May support targeted gene therapy for MI; extends preclinical synergy data but leaves translation open.
Does coexpression of VEGF and Ang1 improve cardiac function and perfusion in a porcine model of myocardial infarction?
Cardiac-specific and hypoxia-induced coexpression of VEGF and Ang1 improves perfusion and function in a porcine MI model by inducing angiogenesis and cardiomyocyte proliferation while reducing apoptosis.
Tao et al. (2011) studied Myocardial infarction. AAV-MLCVEGF and AAV-MLCAng1 coinjection vs. AAV-CMVLacZ or saline was evaluated on Cardiac function, myocardial perfusion, angiogenesis, cardiomyocyte proliferation, and apoptosis. Coinjection of AAV vectors expressing VEGF and Ang1 improved cardiac perfusion and function in a porcine myocardial infarction model by inducing angiogenesis and reducing apoptosis.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: