| Abstract [eng] |
Cardiovascular diseases are the most common reason for death worldwide. They have heterogenous pathophysiologic mechanisms, including augmented oxidative stress, inflammation and activated contact and complement systems. Surplus levels of reactive oxygen species induce damage to cellular macromolecules such as deoxyribonucleotide acid, 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. In addition, contact and complement systems are involved in coagulation and inflammatory processes that can contribute to the atherosclerotic and thrombotic environment, leading to cardiovascular diseases. Improved knowledge of biomolecular processes triggered by oxidative stress, contact, and complement systems would aid in developing tools for assessing cardiovascular diseases and applying them in clinical settings. Still, some research gaps should be filled by defining the most clinically relevant biomarkers for oxidative stress, contact and complement systems with high sensitivity and specificity for cardiovascular diseases. This work seeks to review the literature on thromboinflammation caused by oxidative stress, contact, and complement systems that lead to cardiovascular diseases and to describe potential biomarkers for estimating the risk and improving diagnosis and potential treatment of cardiovascular diseases targeting oxidative stress, contact and complement systems. |
