Oxidative Stress and Its Role in Vascular Damage and Atherosclerosis

Oxidative stress (OS), resulting from an imbalance between reactive oxygen species (ROS) generation and antioxidant defenses, plays a pivotal role in vascular diseases such as atherosclerosis and hypertension. ROS derived from NADPH oxidase, mitochondria, and xanthine oxidase promote endothelial dysfunction by inducing lipid and protein oxidation, apoptosis, and pro-inflammatory signaling, thereby enhancing smooth muscle proliferation and atherogenesis. This review summarizes the molecular mechanisms linking OS to vascular injury and highlights the interplay between ROS and inflammation in the progression of cardiovascular disease. Particular attention is given to biomarkers of oxidative stress, including those assessing antioxidant enzyme activity and oxidative damage products, which hold potential for clinical use. However, challenges remain regarding their standardization and variability influenced by biological and environmental factors. Therapeutic strategies targeting OS, including dietary and pharmacological antioxidants, show promise in improving vascular health, although clinical outcomes have been inconsistent. Personalized approaches based on accurate redox profiling may enhance efficacy. Overall, OS is a central mediator in vascular pathology, and progress in biomarker validation and targeted therapies will be essential to translate current knowledge into effective prevention, diagnosis, and treatment of cardiovascular diseases.