There is overwhelming evidence for an involvement of reactive oxygen species (ROS) in the pathogenesis of diabetes-associated
vascular complications. However, neither the exact source of the ROS initiating cascades leading to cell dysfunction in diabetes
nor their chemical nature is fully understood. Furthermore, despite our knowledge of the crucial role of ROS in diabetes,
little is known about the actual targets and the molecular consequences of the interaction of ROS with cellular signalling
pathways.
Keywords Diabetes - reactive oxygen species - superoxide - nitric oxide - RhoA - Rac - tyrosine kinases - serine/threonine kinases - Ca2+-homeostasis - NF-ϰB - NFAT - AP-1 - matrix metalloproteinases.
Received: 29 August 2001 and in revised form:17 December 2001