English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

In recent years, there has been intense interest in vascular NAD(P)H oxidases and their role in vascular injury and atherosclerosis. Balloon injury has been shown to cause large increases in O2– stemming from NAD(P)H oxidases,1 while other studies have shown that hypercholesterolemia and atherosclerosis can induce vascular expression of NADPH oxidase.2 3 4 This induction has been implicated in cell phenotype change and proliferation, and a similar process can be inferred to occur during vascular grafting.5 Two key studies have demonstrated that overexpression of NAD(P)H oxidase in cells leads to transformation to a proliferative phenotype,6 7 and various redox mechanisms transducing this transformation in injury have been elucidated.8 On the contrary, other reports have shown that deletion of 2 essential components of phagocyte NAD(P)H oxidase fail to inhibit lesion formation in apoE–/– mice.9 10 However, it remains to be determined whether those components and NAD(P)H oxidase do play a role under conditions in which the renin-angiotensin system is activated.11 12 In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , West et al13 present exciting findings suggesting a role for NAD(P)H oxidase–expressing cells in intimal hyperplasia after venous bypass. The authors performed elegant immunohistochemical analyses in an attempt to carefully determine the source and state of differentiation of cells in the subintimal space. They found that cells that strongly express p22 phox (an essential NADPH oxidase component) do not express smoothelin, a marker for highly differentiated smooth muscle cells.14 Their intriguing results show that whereas most cells in the neointima are positive for α-actin, desmin, and smoothelin (all markers for smooth muscle cells) and yet weakly positive for p22 phox , those that strongly express p22 phox do not express desmin or smoothelin. These data suggest that there …

NAD(P)H Oxidase: Marker of the Dedifferentiated Neointimal Smooth Muscle Cell?