Abstract
See related article, pp 1225–1231 Aging progressively narrows the functional reserve of several organs and tissues, in association with variable degrees of morphological changes. Current views strongly indicate that resident stem and progenitor cells contribute to tissue homeostasis throughout life in virtually all organs and tissues, even those traditionally considered as postmitotic. In the aging human heart, the progressive loss of cardiomyocytes is balanced by an increased myocyte turnover through cardiac stem cells.1 However, this balance is compromised, and net cardiomyocyte loss is accelerated when cardiovascular risk factors are present, either nonmodifiable, such as male sex,1 or modifiable, such as diabetes mellitus.2 Similarly, an endothelial damage is normally repaired by resident endothelial cells and endothelial progenitors (EPCs), but this mechanism is impaired by cardiovascular risk factors and age, per se.3 Several authors have documented that bone marrow-derived EPCs from aged animals or humans are quantitatively reduced and dysfunctional,4,5 thus predisposing to atherosclerosis. This has important pathophysiological and therapeutic implications, because autologous EPCs are being used in cell therapy trials that often involve aging individuals. Aging is a major determinant of bone marrow function, which can explain the reduced EPC levels in the elderly. On the other …
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