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This editorial refers to ‘Involvement of vascular peroxidase 1 in angiotensin II-induced vascular smooth muscle cell proliferation’ by Ruizheng Shi et al ., doi:10.1093/cvr/cvr042 Many cell culture and animal studies suggest that an increased formation of reactive oxygen species (ROS) promotes smooth muscle cell proliferation and matrix formation. It is therefore believed that increased ROS production contributes to such different entities as hypertension, restenosis, or arteriosclerosis. Initially, redox processes were believed to be mediated predominantly by hydrogen peroxide (H2O2). Over the years, however, many new aspects of redox signalling have been identified such as delicate alterations in the thiol redox state affecting the cellular redox potential, the complex interplay of nitric oxide with ROS, including the subsequent formation of peroxynitrite, and finally the involvement of peroxidases in redox signalling.1Peroxidases catalyse the oxidation of a broad spectrum of substrates by H2O2, which, in the case of thyroid peroxidase, is needed for the oxidation of iodine and the formation of thyroid hormone (TPO), or in the case of myeloperoxidase (MPO) results in the formation of hypochlorous acid (HOCl), an important mediator of host defense.2 In the cardiovascular system, MPO contributes to vascular dysfunction; it promotes lipid peroxidation, scavenges nitric oxide and MPO products activate matrix metalloproteinases, promoting tissue remodelling that can result in atrial fibrillation.3In addition to TPO and MPO, lactoperoxidase, eosinophil peroxidase, and salivary peroxidase belong to the …

Vascular peroxidase 1/peroxidasin: a complex protein with a simple function?