Effects of physical activity on endothelial progenitor cells (EPCs)

Abstract

Physical activity has a therapeutic role in cardiovascular disease (CVD), through its beneficial effects on endothelial function and cardiovascular system. Circulating endothelial progenitor cells (EPCs) are bone marrow (BM) derived cells that represent a novel therapeutic target in CVD patients, because of their ability to home to sites of ischemic injury and repair the damaged vessels. Several studies show that physical activity results in a significant increase in circulating EPCs, and, in particular, there are some evidence of the beneficial exercise-induced effects on EPCs activity in CVD settings, including coronary artery disease (CAD), heart failure (HF), and peripheral artery disease (PAD). The aim of this paper is to review the current evidence about the beneficial effects of physical exercise on endothelial function and EPCs levels and activity in both healthy subjects and patients with CVD.

Exercise and Stem Cells

“…In general, acute exercise is associated with an increase in appearance of CACs in the blood of healthy volunteers, 37 patients with CVD risk factors, 74 and patients with established CVD 75 although the acute response varies according to CAC subtype, and exercise type, duration, and intensity as well as disease status (Table 2). 43,75 With a standard acute bout of moderate to intense exercise (30-45 min), maximal, or symptom-limited treadmill or bicycle tests, CACs are mobilized quickly, demonstrating significant increases from rest within approximately 10-30 min following exercise completion and returning to resting levels within 24 h. In patients with heart failure, the mobilization of CD34 + KDR + was smaller and returned to baseline more quickly than healthy subjects.…”

“…The effect of acute exercise and exercise training on CACs has been recently reviewed elsewhere. [73][74][75] The focus of the following is a review of the effect of exercise on CACs, highlighting studies that lend novel insight into the CAC response to exercise or potential mechanisms to explain the role of exercise to change CAC characteristics.…”

Serum uric acid as a metabolic regulator of endothelial reparative processes in heart failure patients

“…It is well known that STAT (signal transducer and activator of transcription) especially STAT-3 is an acute-phase response factor, which is activated by various cytokines and growth factors including interleukin (IL)-5, IL6, and interferon γ. Through expression of a variety of genes in response to cell stimuli, MPCs may differentiate into mater endothelial cells and thereby contribute in cellular processes such as endothelial cell growth, apoptosis, angiogenesis, and vasculature reparation [39] . In fact, number and migratory activity of MPCs obtained from CHF patients demonstrated low capacity to differentiation after stimulation of potent pro-angiogenic factors, such as fibroblast growth factor-4 and vascular endothelial growth factor, and as well as decreased resistance to hypoxic stress conditions [40] .…”

Physical activity and progenitor cell-mediated endothelial repair in chronic heart failure: Is there a role for epigenetics?

“…Regular physical activity (PA) has finally been accepted as a highly effective and safe treatment for CHF (Coats, 2011) and as a potent stimulus for endogenous endothelial repair mechanisms (De Biase et al, 2014). A number of studies have suggested that PA can enhance endothelial renewal, largely through the mobilization of bone marrow (BM)-derived EPCs and CACs (Van Craenenbroeck et al, 2010a, 2010b.…”