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Cardiovascular diseases are the most common reason for death worldwide, with heterogeneous pathophysiologic mechanisms. Augmented oxidative stress is a potential etiology of cardiovascular diseases induced by surplus levels of reactive oxygen species, which yield damage to cellular macromolecules such as DNA, proteins, and lipids. Increased reactive oxygen species result in decreased nitric oxide availability, vasoconstriction and the development of pro- coagulant and pro-inflammatory states in blood vessels. This review seeks to introduce oxidative stress in cardiovascular diseases, focusing on endothelial dysfunction caused by oxidative stress and manifesting as a mechanism of thromboinflammation in the vasculature that leads to cardiovascular diseases.
Julija Valaitienė (Wed,) studied this question.