Physical activity and progenitor cell-mediated endothelial repair in chronic heart failure: Is there a role for
Rina Recchioni1, Fiorella Marcheselli1, Roberto Antonicelli2
1Center of Clinical Pathology and Innovative Therapy, Italian National Research Center on Aging (INRCA-IRCCS), Ancona, Italy.
Insights
Exercise may improve heart function in elderly patients with chronic heart failure (CHF) by boosting endothelial progenitor cells (EPCs) and circulating angiogenic cells (CACs). These benefits might be linked to epigenetic changes, offering new therapeutic avenues for CHF.
Area of Science:
- Cardiovascular Medicine
- Cell Biology
- Epigenetics
Background:
- Chronic heart failure (CHF) significantly impacts the elderly, with endothelial dysfunction playing a key role in its progression.
- Endothelial progenitor cells (EPCs) and circulating angiogenic cells (CACs) are crucial for repairing blood vessel damage and counteracting endothelial dysfunction.
- Exercise is recognized as a therapeutic strategy for CHF, enhancing endothelial renewal via EPC and CAC mobilization.
Purpose of the Study:
- To review the role of EPCs and CACs in endothelial repair in CHF patients.
- To examine the impact of exercise training on EPCs and CACs in CHF.
- To explore the potential role of epigenetic modifications, such as DNA methylation and microRNAs, in mediating exercise effects on endothelial repair in CHF.
Main Methods:
- Literature review of studies on EPCs, CACs, exercise training, and epigenetic modifications in CHF.
- Analysis of current knowledge regarding endothelial repair mechanisms in CHF.
- Synthesis of evidence linking exercise-induced epigenetic changes to endothelial function.
Main Results:
- Exercise training enhances endothelial renewal by mobilizing bone marrow-derived EPCs and CACs in CHF patients.
- Emerging evidence suggests exercise training induces epigenetic modifications, including DNA methylation and microRNA expression changes.
- Dysregulation of miRNAs involved in endothelial function is observed in CHF patients.
Conclusions:
- EPCs and CACs are vital for endothelial repair in CHF, and exercise effectively promotes their mobilization.
- Epigenetic mechanisms, particularly those involving miRNAs, may mediate some of the beneficial effects of exercise on endothelial repair in CHF.
- Further research into exercise-induced epigenetic modifications could reveal novel therapeutic targets for managing CHF.
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.
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