Mitochondrial redox plays a critical role in the paradoxical effects of NAPDH oxidase-derived ROS on coronary endothelium

Conclusion</div>The findings suggest that NOX-derived ROS results in increased mito-ROS. Whereas short-term increase in mito-ROS was counteracted by MnSOD, long-term increase in ROS resulted in nitrotyrosine-mediated inactivation of MnSOD, leading to unchecked increase in mito-ROS and loss of Δ<span style="font-style:italic;">ψ</span>m followed by inhibition of endothelial function and proliferation.</span>
Source: Cardiovascular Research - Category: Cardiology Source Type: research