Why the study?
Endothelial progenitor cells contribute to endothelial homeostasis and are impaired in the elderly, but their role in frailty required illustration.
This review highlights the pathophysiological role of endothelial progenitor cell impairment in frailty and age-related endothelial dysfunction.
EPC impairment may underlie frailty; hypothesis-generating for targeted interventions in age-related endothelial dysfunction.
Frailty is a clinical condition closely related to aging which is characterized by a multidimensional decline in biological reserves, a failure of physiological mechanisms and vulnerability to minor stressors. Chronic inflammation, the impairment of endothelial function, age-related endocrine system modifications and immunosenescence are important mechanisms in the pathophysiology of frailty. Endothelial progenitor cells (EPCs) are considered important contributors of the endothelium homeostasis and turn-over. In the elderly, EPCs are impaired in terms of function, number and survival. In addition, the modification of EPCs' level and function has been widely demonstrated in atherosclerosis, hypertension and diabetes mellitus, which are the most common age-related diseases. The purpose of this review is to illustrate the role of EPCs in frailty. Initially, we describe the endothelial dysfunction in frailty, the response of EPCs to the endothelial dysfunction associated with frailty and, finally, interventions which may restore the EPCs expression and function in frail people.
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Komici et al. (2023) studied this question.
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