Purpose of review: Reactive oxygen species have been implicated in the initiation and progression of atherosclerosis. Reactive oxygen species can oxidize lipoproteins, limit the vascular availability of antiatherosclerotic nitric oxide and promote vascular expression of cytokines and adhesion molecules. Nox proteins of the NADPH oxidase family are prominent sources of vascular reactive oxygen species, and Nox protein-dependent reactive oxygen species production has been linked to atherogenesis. Recently, significant progress has been made in the understanding of differences among the Nox proteins.
Recent findings: Nox proteins exhibit cell-specific expression patterns and divergent molecular mechanisms controlling activity have been identified for individual Nox proteins. These aspects may relate to cellular activation, differentiation, proliferation, angiogenesis and gene expression, and may also be modulated by the functional states of the vessel such as endothelial dysfunction: in quiescent vessels, Nox proteins contribute to signal transduction and to the physiological responses to growth factors such as vascular endothelial growth factor or thrombin. Excessive Nox-dependent reactive oxygen species formation in vascular disease such as hyperlipidemia or diabetes, however, largely contributes to vascular dysfunction resulting in defective angiogenesis and inflammatory activation.
Summary: Reactive oxygen species, specifically generated by individual Nox proteins, act as secondary messengers. Selective inhibition of Nox proteins might be a novel approach to prevent and treat cardiovascular diseases.