INTRODUCCIÓN: REVISIÓN CRITICA DEL PROBLEMA

Conclusions
ANEXOS
Our data suggest that gHSA-enhanced ROS production in HUVEC is the result of
the stimulation of two different sources of ROS. In one hand, by an unknown
mechanism, gHSA uncouples eNOS, promoting ROS production instead of NO. In
the other hand, gHSA activates NF-κB and promotes NOX4 and P22PHOX, two
subunits of NADPH oxidase, the main source of ROS in the endothelium.
Furthermore, we observed that AP-1 is a main transcription factor controlling
NADPH oxidase and eNOS expression in human endothelial cells. The inhibition
of this factor translates a marked increase in ROS production. All these results
open new ways to the investigation of the causes of endothelial dysfunction in
cardiovascular diabetic complications.
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