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

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)71-80
Number of pages10
JournalMechanisms of Ageing and Development
Volume159
DOIs
Publication statusPublished - Oct 2016

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Epigenomics
Heart Failure
Exercise
MicroRNAs
Histone Code
Untranslated RNA
DNA Methylation
Plasma Cells
Disease Progression
Heart Diseases
Endothelial Cells
Bone Marrow
Endothelial Progenitor Cells
Mortality
Therapeutics

Keywords

  • Review
  • Journal Article

Cite this

@article{203e487e57a040a188bf71564d76b06b,
title = "Physical activity and progenitor cell-mediated endothelial repair in chronic heart failure: Is there a role for epigenetics?",
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.",
keywords = "Review, Journal Article",
author = "Rina Recchioni and Fiorella Marcheselli and Roberto Antonicelli and Raffaella Lazzarini and Emanuela Mens{\`a} and Roberto Testa and Procopio, {Antonio Domenico} and Fabiola Olivieri",
note = "Copyright {\circledC} 2016 Elsevier Ireland Ltd. All rights reserved.",
year = "2016",
month = "10",
doi = "10.1016/j.mad.2016.03.008",
language = "English",
volume = "159",
pages = "71--80",
journal = "Mechanisms of Ageing and Development",
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T1 - Physical activity and progenitor cell-mediated endothelial repair in chronic heart failure

T2 - Is there a role for epigenetics?

AU - Recchioni, Rina

AU - Marcheselli, Fiorella

AU - Antonicelli, Roberto

AU - Lazzarini, Raffaella

AU - Mensà, Emanuela

AU - Testa, Roberto

AU - Procopio, Antonio Domenico

AU - Olivieri, Fabiola

N1 - Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

PY - 2016/10

Y1 - 2016/10

N2 - 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.

AB - 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.

KW - Review

KW - Journal Article

U2 - 10.1016/j.mad.2016.03.008

DO - 10.1016/j.mad.2016.03.008

M3 - Article

C2 - 27015708

VL - 159

SP - 71

EP - 80

JO - Mechanisms of Ageing and Development

JF - Mechanisms of Ageing and Development

SN - 0047-6374

ER -