Endothelial Progenitor Cells and Cardiovascular Correlates

Abstract

Cardiovascular disease is cited as the underlying cause of death in one out of every three deaths within the United States; this burden on the health care system percolates down to affect patients on an individual level. In part, the problem arises from the low regenerative capacity of cardiovascular system cells, for example, cardiac myocytes, and from oxidative stressors to the human body. Endothelial progenitor cells (EPCs) are a type of stem cell, and various clinical conditions including hypertension and renal failure underlie their dysfunction. EPCs are classified as either early or late outgrowth endothelial progenitor cells depending on the time they appear in circulation and at the site of injury after an inciting event. Their function is paracrine through the release of cytokines, growth factors and chemokines such as interleukin-6 and vascular endothelial growth factor, and they are involved in transdifferentiation into vascular smooth muscle cells and potentially cardiac myocytes. They are beneficial to the modification of cardiovascular cell apoptosis, fibrosis, and contractility. In times of stress, the normal function of endothelial progenitor cells is altered; this creates a maladaptive cycle where stress and failed coping mechanisms enhance each other toward the culmination of cardiovascular disease. The development of the cardiovascular system follows gastrulation in the embryonic period, and the cells that form the system are derived from the mesoderm; being mesoderm, the vascular cells exhibit heterogeneity in their origin and function. The need to understand the molecular and cellular regulatory pathways during development can amalgamate efforts of endothelial cell and cardiovascular system pathophysiology for the advancement of patient cardiovascular reserve and function.