Abstract

See related article, pages 314–322 The formation of coronary collateral vessels constitutes a compensatory adaptation of the heart to ischemia. This vascular response increases blood supply to the myocardium reducing the area of hypoxic damage and, ultimately, infarct size. The recruitment of collateral vessels within the coronary circulation is favored by multiple episodes of ischemia, which provide the stimuli necessary for the growth of vascular structures and increased blood flow. The degree of collateralization significantly influences the prognosis of an ischemic episode, which is more severe with diabetes, metabolic syndrome, or in the elderly, the patient population mostly affected by coronary artery disease.1 Originally, angiogenesis, ie, sprouting of vessels from the preexisting circulation, was considered the exclusive mechanism of vascular remodeling and growth. The identification of circulating endothelial progenitor cells (EPCs) has modified this view.2 Migration and homing of EPCs to ischemic regions leads to de novo formation of vascular structures. In analogy with vessel development in the embryo, this process has been called vasculogenesis. Also, circulating EPCs participate in reendothelization of damaged vessels, together with resident vascular progenitor cells.3 EPCs represent a heterogeneous cell population of multiple origins and distinct phenotypes, which are able to give rise to functionally competent endothelial cells.4 In the hierarchy established in the hematopoietic system, progenitors identify cells with lower differentiation potential than stem cells (SCs). However, EPCs possess degrees of stemness, which include self-renewal, clonogenicity, and differentiation capacity.4 EPCs represent various subsets of progenitor cells that have distinct phenotypes but share the ability to differentiate into mature endothelial cells. During embryogenesis, hematopoietic cells and endothelial cells develop temporally and spatially in close association. Blood cells are surrounded by layers of endothelial cells suggesting a joint origin of these lineages from a common precursor, the embryonic hemangioblast.4 …

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