Exercise Training Effects on Circulating Endothelial and Progenitor Cells in Heart Failure.
Christos KourekAlexandros BriasoulisVirginia ZouganeliEleftherios KaratzanosSerafim NanasStavros DimopoulosPublished in: Journal of cardiovascular development and disease (2022)
Heart failure (HF) is a major public health issue worldwide with increased prevalence and a high number of hospitalizations. Patients with chronic HF and either reduced ejection fraction (HFrEF) or mildly reduced ejection fraction (HFmrEF) present vascular endothelial dysfunction and significantly decreased circulating levels of endothelial progenitor cells (EPCs). EPCs are bone marrow-derived cells involved in endothelium regeneration, homeostasis, and neovascularization. One of the unsolved issues in the field of EPCs is the lack of an established method of identification. The most widely approved method is the use of monoclonal antibodies and fluorescence-activated cell sorting (FACS) analysis via flow cytometry. The most frequently used markers are CD34, VEGFR-2, CD45, CD31, CD144, and CD146. Exercise training has demonstrated beneficial effects on EPCs by increasing their number in peripheral circulation and improving their functional capacities in patients with HFrEF or HFmrEF. There are two potential mechanisms of EPCs mobilization: shear stress and the hypoxic/ischemic stimulus. The combination of both leads to the release of EPCs in circulation promoting their repairment properties on the vascular endothelium barrier. EPCs are important therapeutic targets and one of the most promising fields in heart failure and, therefore, individualized exercise training programs should be developed in rehabilitation centers.
Keyphrases
- heart failure
- public health
- acute heart failure
- flow cytometry
- skeletal muscle
- nitric oxide
- left ventricular
- stem cells
- endothelial cells
- induced apoptosis
- risk factors
- vascular endothelial growth factor
- single cell
- single molecule
- cardiac resynchronization therapy
- cell therapy
- cell proliferation
- bone marrow
- signaling pathway
- chemotherapy induced
- endoplasmic reticulum stress