T Inhibition of Endostatin / Collagen XVIII Deteriorates Left Ventricular Remodeling and Heart Failure in Rat Myocardial Infarction Model

herapeutic angiogenesis aims to increase coronary collateralization, which improves the prognosis of patients after myocardial infarction (MI) and other obstructive coronary artery diseases (CAD). Collaterals limit infarct size and improve ventricular function and overall perfusion in the ischemic myocardium.1,2 The development of coronary collaterals appears to be initiated by an occlusive event, resulting in opening of preexisting anastomotic channels through increased shear forces and pressure or by formation of novel capillary sprouts (angiogenesis) from the ischemic area.3 Subsequent maintenance and maturation of these vessels (arteriogenesis) is believed to be mediated by a balance of proand anti-angiogenic factors that favor neovascularization.3 The concept of using the genes or proteins of pro-angiogenic growth factors (eg, vascular endothelial growth factor) for therapeutic angiogenesis is well established and currently being tested in clinics. On the other hand, the role of endogenous angiogenesis inhibitors in angiogenesis in ischemic heart disease and subsequent disease pathology and prognosis has been poorly investigated.