Table 1.

Nox enzymes in the vasculature

nox member	localization	ROS type	regulators	expression	activation	cardiovascular physiology	cardiovascular pathophysiology
Nox1	transmenbrane caveolae endosomes	superoxide anion	p22phox p47phox, Noxa1, Rac or Noxo1, Noxa1, Rac	smooth muscle cells epithelial cells, uterus osteoclasts, neurons	stimulus induced Ang II, PDGF, FGF	proliferation, migration extracellular matrix production host defense	vascular hypertrophy hypertension, vascular injury diabetes
Nox2	phagosomes caveolae endosomes	superoxide anion	p22phox, p47phox, p67phox, p40phox rac	endothelial cells cardiomyocytes, hepatocytes fibroblastes, phagocytes neurons, skeletal muscle myocytes	agonist-induced (Ang II, VEGF, TNFα, endothelin1) mechanical forces	angiogenesis apoptosis, oxygen sensing inflammation	hypoxia, diabetes hypercholesterolemia pulmonary hypertension
Nox3	plasma membrane	superoxide anion	p22phox, Noxo1 possibly Noxa1, Rac	inner ear lung endothelial cells hepatocytes	agonist-induced (TNFα) constitutively active	unknown	insulin resistance
Nox4	focal adhesion nucleus endoplasmic reticulum	hydrogen peroxide	p22phox Poldip2	mesangial cells, smooth muscle endothelial cells, fibroblasts keratinocytes, osteoclasts neurons, hepatocytes cardiomyocytes	constitutively active stimulus induced (TGFβ, IL-1, Vit.D, thrombin, ER stressors)	senescence, apoptosis endoplasmic reticulum stress survival, differentiation oxygen sensing cytoskeletal regulation	hypertrophy pulmonary hypertension/fibrosis metabolic syndrome
Nox5	internal membranes plasma membrane	superoxide	calcium	endothelial cells smooth muscle cells testes, spleen	calcium activated	proliferation inflammation	unknown