 Oxidative stress is a common mediator in pathogenicity of established cardiovascular risk factors. It likely mediates effects of emerging, less well-defined variables that contribute to residual risk, not explained by traditional factors. Functional oxidative modifications of cellular proteins, both reversible and irreversible, are a causal step in cellular dysfunction. Identifying markers of oxidative stress has been the focus of many researchers as they have the potential to act as an integrator of a multitude of processes that drive cardiovascular pathobiology. One of the major challenges is the accurate quantification of reactive oxygen species with very short half-life. Redux-sensitive proteins with important cellular functions are confined to signaling microdomains in cardiovascular cells and are not readily available for quantification. A popular approach is the measurement of stable byproducts modified under conditions of oxidative stress that have entered the circulation. However, these may not accurately reflect redox stress at the cell-slash-tissue level. Many of these modifications are functionally silent. Functional significance of the oxidative modifications enhances their validity. This article was authored by Edwin Ho, Kivan Karimi Golugahi, Chia Chi Lu, and others. We are article.tv, links in the description below.