16 124 897 livres à l’intérieur 175 langues
2 047 051 livres numériques à l’intérieur 101 langues
Cela ne vous convient pas ? Aucun souci à se faire ! Vous pouvez renvoyer le produit dans les 30 jours
Impossible de faire fausse route avec un bon d’achat. Le destinataire du cadeau peut choisir ce qu'il veut parmi notre sélection.
Politique de retour sous 30 jours
Reactive oxygen species (ROS) influence various physiological processes including host defense, hormone biosynthesis, and cellular signaling. Increased ROS production (oxidative stress) is implicated in many diseases of the cardiovascular system, including hypertension, atherosclerosis, cardiac failure, stroke, diabetes, and kidney disease. ROS are produced throughout the cardiovascular system, in the kidney and central and peripheral nervous system. A major source for cardiovascular, renal, and neural ROS is a family of non-phagocytic NAD(P)H oxidases, including the prototypic Nox2 homologue-based NAD(P)H oxidase, as well as other NAD(P)H oxidases, such as Nox1 and Nox4. Other possible sources include mitochondrial electron transport enzymes, xanthine oxidase, cyclooxygenase, lipoxygenase, and uncoupled nitric oxide synthase (NOS). NAD(P)H oxidase-derived ROS is important in regulating endothelial function and vascular tone and oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in cardiovascular disease. These findings have evoked considerable interest because of the possibilities that therapies targeted against non-phagocytic NAD(P)H oxidase to decrease ROS generation and/or strategies to increase nitric oxide (NO) availability and antioxidants may be useful in minimizing vascular injury and thereby prevent or regress target organ damage associated with hypertension and other cardiovascular diseases.