Physical activity and progenitor cell-mediated endothelial repair in chronic heart failure: Is there a role for epigenetics?. (October 2016)

• Record Type: Journal Article
• Authors: Recchioni, Rina; Marcheselli, Fiorella; Antonicelli, Roberto; Lazzarini, Raffaella; Mensà, Emanuela; Testa, Roberto; Procopio, Antonio Domenico; Olivieri, Fabiola
• Is Part Of: Mechanisms of ageing and development. Volume 159(2016)
• Page Start: 71
• Page End: 80
• Publication Date: 2016-10
• Subjects: Epigenetics -- Endothelial progenitor cell -- Chronic heart failure -- Physical activity -- microRNA; Aging -- Periodicals; Developmental biology -- Periodicals; Aging -- Periodicals; Developmental Biology -- Periodicals; Vieillissement -- Périodiques; Biologie du développement -- Périodiques; Aging; Developmental biology; Periodicals; 612.67
• DOI: 10.1016/j.mad.2016.03.008
• Languages: English
• ISSNs: 0047-6374

Abstract

Highlights: Regular physical activity has been accepted as a highly effective and safe treatment for chronic heart failure (CHF). Exercise training (ET) promotes endothelial repair mechanisms in CHF by mobilization of progenitor cells from BM, increasing their number and improving angiogenic properties. The molecular mechanisms underlying the positive effects of physical activity on endothelial repair mechanisms in CHF patients are not completely known. The effects of ET on endothelial repair mechanisms in CHF elderly patients could be mediated by epigenetic mechanisms. Abstract: Chronic heart failure (CHF) is the most common cardiac disease among the elderly and a leading cause of mortality in elderly patients. Endothelial dysfunction is held to have a major role in the development and progression of CHF, which results in progressively impaired functional capacity. Endothelial progenitor cells (EPCs) and circulating angiogenic cells (CACs) are the main players involved in the endogenous repair mechanisms that can counteract endothelial dysfunction. A mounting body of data indicates that exercise enhances endothelial renewal through mobilization of bone marrow-derived EPCs and CACs, making it an effective therapeutic tool for CHF. Interestingly, emerging evidence has been showing that exercise training can also promote epigenetic modifications, e.g. DNA methylation, histone modifications, and differential expression of specific non-coding RNAs like microRNA (miRNAs). Since deregulation of the miRNAs involved in endothelial function modulation has widely been documented in circulating cells and plasma of CHF patients, deregulation of epigenetic features could play a key role in disease progression. Here, we review current knowledge of the contribution of EPCs and CACs to endothelial repair mechanisms in CHF patients, focusing on the effects induced by exercise training and hypothesizing that some of these effects can be mediated by epigenetic mechanisms.