Hyperglycemia-induced reactive oxygen species and impaired endothelial progenitor cell function.

Abstract:

:Vascular complications in diabetes are a significant source of human morbidity and mortality, affecting multiple organ systems and persisting despite tight glucose control. Many of these complications can be linked to impairments in vasculogenesis, the process by which circulating and bone marrow-derived endothelial progenitor cells (EPCs) contribute to new vessel formation. Recent evidence suggests that hyperglycemia alone, through the mitochondrial overproduction of reactive oxygen species (ROS), can induce changes in gene expression and cellular behavior in diabetes. In this review, we examine how hyperglycemia-induced overproduction of ROS could explain EPC impairments observed in diabetes. Experimentally, impairments in EPC function prevent new blood vessel growth and are potentially reversible by manipulations to decrease ROS. Novel strategies aimed at reducing hyperglycemia-induced ROS may be a useful adjuvant to antihyperglycemic therapies in the restoration of vasculogenesis and the prevention of diabetic complications.

journal_name

Antioxid Redox Signal

authors

Callaghan MJ,Ceradini DJ,Gurtner GC

doi

10.1089/ars.2005.7.1476

keywords:

subject

Has Abstract

pub_date

2005-11-01 00:00:00

pages

1476-82

issue

11-12

eissn

1523-0864

issn

1557-7716

journal_volume

7

pub_type

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