TWEAK/Fn14 interaction promotes oxidative stress through NADPH oxidase activation in macrophages

Conclusions Our results suggest that TWEAK regulates vascular damage by stimulating ROS production in an Nox2-dependent manner. These new insights into the TWEAK/Fn14 axis underline their potential use as therapeutic targets in atherosclerosis.
Source: Cardiovascular Research - Category: Cardiology Authors: Tags: Vascular biology Source Type: research