Vascular Disease as a Consequence of Impaired Endothelial Redox Adaptation

Endothelial dysfunction plays a central role in cardiovascular and cerebrovascular disease, but its portrayal as a simple imbalance associated with oxidative stress and nitric oxide (NO) deficiency has somewhat hindered therapeutic progress over the years.Accumulating evidence supports a conceptual shift towards endothelial redox plasticity, the capacity of vascular endothelium to dynamically regulate NO synthase activity and reactive oxygen species (ROS) production during various physio-pathological processes, including growth, repair, and ageing.Experimental, genetic, and clinical data exhibit that ROS are required for physiological adaptation, and that pathology emerges from a regulatory imbalance rather than oxidative stress alone.Mechanistic studies have further exhibited that redox-sensitive signalling networks tightly coordinate endothelial survival, mitochondrial function, and inflammatory activation, reinforcing the concept that oxidative signalling is integral to vascular homeostasis rather than merely deleterious.Distinct vessel-specific redox profiles, microenvironmental factors, progenitor cell dysfunction, and cellular senescence further determine vascular resilience.Hence, restoration of redox adaptability offers a sound foundation for precision vascular therapies.