Publication Date:
2012
abstract:
Bone-marrow-derived cells-mediated postnatal vasculogenesis has been reported as the main responsible for the regulation of
vascular homeostasis in adults. Since their discovery, endothelial progenitor cells have been depicted as mediators of postnatal
vasculogenesis for their peculiar phenotype (partially staminal and partially endothelial), their ability to differentiate in endothelial
cell line and to be incorporated into the vessels wall during ischemia/damage. Diabetes mellitus, a condition characterized by
cardiovascular disease, nephropathy, and micro- and macroangiopathy, showed a dysfunction of endothelial progenitor cells.
Herein, we review the mechanisms involved in diabetes-related dysfunction of endothelial progenitor cells, highlighting how
hyperglycemia affects the different steps of endothelial progenitor cells lifetime (i.e., bonemarrowmobilization, trafficking into the
bloodstream, differentiation in endothelial cells, and homing in damaged tissues/organs). Finally, we review preclinical and clinical
strategies that aim to revert diabetes-induced dysfunction of endothelial progenitor cells as a means of finding new strategies to
prevent diabetic complications.
vascular homeostasis in adults. Since their discovery, endothelial progenitor cells have been depicted as mediators of postnatal
vasculogenesis for their peculiar phenotype (partially staminal and partially endothelial), their ability to differentiate in endothelial
cell line and to be incorporated into the vessels wall during ischemia/damage. Diabetes mellitus, a condition characterized by
cardiovascular disease, nephropathy, and micro- and macroangiopathy, showed a dysfunction of endothelial progenitor cells.
Herein, we review the mechanisms involved in diabetes-related dysfunction of endothelial progenitor cells, highlighting how
hyperglycemia affects the different steps of endothelial progenitor cells lifetime (i.e., bonemarrowmobilization, trafficking into the
bloodstream, differentiation in endothelial cells, and homing in damaged tissues/organs). Finally, we review preclinical and clinical
strategies that aim to revert diabetes-induced dysfunction of endothelial progenitor cells as a means of finding new strategies to
prevent diabetic complications.
Iris type:
1.1 Articolo in rivista
List of contributors:
Alessandra, Petrelli; Raffaele Di, Fenza; Michele, Carvello; Francesca, Gatti; Secchi, Antonio; Paolo, Fiorina
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