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Review
. 2009 Apr 29;302(2):148-58.
doi: 10.1016/j.mce.2008.11.003. Epub 2008 Nov 18.

NADPH oxidases and angiotensin II receptor signaling

Affiliations
Review

NADPH oxidases and angiotensin II receptor signaling

Abel Martin Garrido et al. Mol Cell Endocrinol. .

Abstract

Over the last decade many studies have demonstrated the importance of reactive oxygen species (ROS) production by NADPH oxidases in angiotensin II (Ang II) signaling, as well as a role for ROS in the development of different diseases in which Ang II is a central component. In this review, we summarize the mechanism of activation of NADPH oxidases by Ang II and describe the molecular targets of ROS in Ang II signaling in the vasculature, kidney and brain. We also discuss the effects of genetic manipulation of NADPH oxidase function on the physiology and pathophysiology of the renin-angiotensin system.

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Figures

Figure 1
Figure 1. Structure of the different vascular NADPH oxidases
Different homologues of NADPH oxidases have been found in the vasculature. NoxA1 (NADPH oxidase activator 1) and NoxO1 (NADPH oxidase organizer 1).
Figure 2
Figure 2. Inactivation of protein tyrosine phosphatases (PTP) by H2O2-induced thiol oxidation of cysteine residues
H2O2 can inactivate PTPs either irreversibly (right side) or reversibly (left side). Reactivation of the PTPs requires reduction via thioredoxin (Trx) or glutathione (GSH).
Figure 3
Figure 3. Role of ROS in contraction induced by angiotensin II in vascular smooth muscle cells
ROS production is implicated in calcium dependent and independent induced by angiotensin II. Red lines show inhibitory effects and blue lines depict activation. ROS (reactive oxygen species), AT1R (angiotensin II receptor type 1), PLC (phospholipase C), PIP2 (phosphoinositol biphosphate), IP3 (inositol 1,4,5 triphosphate), IP3R (inositol 1,4,5 triphosphate receptor), SERCA (sarco/endoplasmic reticulum Ca2+-ATPase), GEF (guanine nucleotide exchange factor), GTP (guanosin triphosphate), ROCK (Rho-associate kinase) and MLC (myosin light chain).
Fig 4
Fig 4. Role of ROS in the hypertrophy induced by angiotensin II in vascular smooth muscle cells (left pannel) or messangial cells (right pannel)
Vascular smooth muscle and messangial cells exhibit differences in the targets activated in the hypertrophy induced by angiotensin II. ROS (reactive oxygen species), AT1R (angiotensin II receptor type 1), PKC (protein kinase C), PLD (phospholipase D), PLA2 (phospholipase A2), EGFR (epidermal growth factor receptor), PDGFR (platelet derived growth factor receptor), IGFR (insulin like growth factor receptor) PI3K (phosphatidylinositol 3-kinase), PDK1 (phosphoinositide-dependent protein kinase 1), SHP-2 (Src homology 2 domain-containing protein tyrosine phosphatase), PTEN (phosphatase and tensin homolog), LMW-PTP (low molecular weight phosphatase), p38MAPK (p38 mitogen-activated protein kinase), MAPKAPK-2 (MAPK-activated protein kinase-2), JNK (C-Jun N-terminal kinases), ERK (extracellular signal-regulated kinases), AP-1 (activator protein 1), NF-κβ (nuclear factor-kappa β), CREB (cAMP response element-binding), Ets-1 (E26 transformation-specific sequence), GFLK (Gut-enriched Krüppel-like factor) and COX-2 (ciclooxigenase 2).
Fig 5
Fig 5. Role of ROS in modulation of angiotensin II signaling in the brain
ROS are implicated in the dipsogenic action and blood pressure modulated by angiotensin II in the brain. ROS (reactive oxygen species), AT1R (angiotensin II receptor type 1), PKC (protein kinase C), p38MAPK (p38 mitogen-activated protein kinase) and ERK (extracellular signal-regulated kinases).

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