MMP9 and endothelial dysfunction: Upstream, canonical inflammatory pathways (TNF-α, ROS, macrophage-derived mediators) induce MMP-9 via NF-κB/AP-1 and related pathways, establishing a feed-forward loop in which proteolysis amplifies leukocyte recruitment and oxidative stress, further depressing nitric-oxide bioavailability and vascular reactivity—a hallmark of endothelial dysfunction [53,54,55].