The vascular system delivers blood containing oxygen (O2) and nutrients to tissues according to their local needs. In the finest branches of the vascular tree, capillaries consist of little more than a monolayer of endothelial cells (ECs) surrounded by an extracellular matrix and occasional pericytes. At these sites, microvascular endothelium is in intimate contact with underlying parenchymal cells.
In the heart, capillary ECs lie in close proximity to cardiomyocytes. As a result, significant cross-talk occurs between these two cell types, which involves reciprocal gene regulation, signal transduction, and energy supply (1). Changes in endothelial–myocyte cross-talkmay contribute to and/or arise from numerous cardiac pathologies. In this chapter, we review in vitro and in vivo studies that provide mechanistic insight into the nature of this cell–cell communication.
The endothelium serves as the interface between the circulation and the vascular wall, integrating local and systemic events that regulate vascular function. During embryogenesis, the vascular endothelium is the first cardiovascular cell type to differentiate. These cells provide critical cues to all stages of cardiovascular development, and they are critically involved in myocardial trabeculation and the formation of primitive nutrient vessels.
In the normal heart, the ratio of the number of ECs to cardiac myocytes is approximately three to one (1). Three types of ECs have been identified in the heart based on their location: (a) endocardial ECs, which line the ventricles and atria; (b) myocardial microvascular ECs that line the arterioles, venules, and capillaries of the myocardium; and (c) ECs of epicardial arteries and veins (2–5). Of these, endocardial and microvascular ECs are in closest contact with cardiomyocytes.