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. 2008 Nov 17;107(2):312–323. doi: 10.1093/toxsci/kfn236

FIG. 1.

FIG. 1.

Hypothetical scheme of arsenic-stimulated redox signaling for vascular cell dysfunction. Arsenic may interact with GPCR to initiate signal amplification schemes regulating NOX-dependent redox signaling. Note that the membrane-bound NOX subunits may more likely reside in intracellular membranes. Downstream signaling for dysfunction was adapted from Lee and Griendling (2008).