NAD(P)H oxidase and renal epithelial ion transport

Schreck, Carlos; O’Connor, Paul

doi:10.1152/ajpregu.00618.2010

Cited by 51 publications

(46 citation statements)

References 49 publications

(64 reference statements)

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“…NADPH oxidase is also the main source of superoxide generation in the mTAL in response to Ang II and increased luminal flow (8,114,274,284). Superoxide generated in the mTAL of the rat kidney activates the PKA signaling pathway and stimulates Na + /K + ATPase and NKCC activity, which subsequently enhances Na + transport and reabsorption (218,284).…”

Section: Medullary Thick Ascending Limbmentioning

confidence: 99%

Oxidant Mechanisms in Renal Injury and Disease

Ratliff

Abdulmahdi

Pawar

et al. 2016

Antioxidants & Redox Signaling

512

513

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Significance: A common link between all forms of acute and chronic kidney injuries, regardless of species, is enhanced generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) during injury/ disease progression. While low levels of ROS and RNS are required for prosurvival signaling, cell proliferation and growth, and vasoreactivity regulation, an imbalance of ROS and RNS generation and elimination leads to inflammation, cell death, tissue damage, and disease/injury progression. Recent Advances: Many aspects of renal oxidative stress still require investigation, including clarification of the mechanisms which prompt ROS/ RNS generation and subsequent renal damage. However, we currently have a basic understanding of the major features of oxidative stress pathology and its link to kidney injury/disease, which this review summarizes. Critical Issues: The review summarizes the critical sources of oxidative stress in the kidney during injury/ disease, including generation of ROS and RNS from mitochondria, NADPH oxidase, and inducible nitric oxide synthase. The review next summarizes the renal antioxidant systems that protect against oxidative stress, including superoxide dismutase and catalase, the glutathione and thioredoxin systems, and others. Next, we describe how oxidative stress affects kidney function and promotes damage in every nephron segment, including the renal vessels, glomeruli, and tubules. Future Directions: Despite the limited success associated with the application of antioxidants for treatment of kidney injury/disease thus far, preventing the generation and accumulation of ROS and RNS provides an ideal target for potential therapeutic treatments. The review discusses the shortcomings of antioxidant treatments previously used and the potential promise of new ones.

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Section: Medullary Thick Ascending Limbmentioning

confidence: 99%

Oxidant Mechanisms in Renal Injury and Disease

Ratliff

Abdulmahdi

Pawar

et al. 2016

Antioxidants & Redox Signaling

512

513

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“…NADPH oxidase is the predominant source of renal O 2 -. NOX proteins are homologs of the phagocytic NADPH oxidase and are distributed widely in the renal vessels, glomeruli, and nephron segments, as summarized in Table 1 (27,88,170,204,254). NOX3 and NOX5 are expressed in the fetal, but not in the adult, kidneys (37).…”

Section: Overview Of Renal Ros and Hypertensionmentioning

confidence: 99%

“…Although NADPH oxidase is the main source of O 2 -in TAL, xanthine oxidase (XO), COX and CYP 450 enzymes also are expressed in this segment and might contribute to O 2 -production (86). NOX2 and p47 phox were identified as the main sources of O 2 -generation in the TAL in response to ANG II or increased luminal flow (114,254,264). Feng et al (62) reported that disruption of the gene for p67 phox decreased medullary NADPH oxidase-dependent O 2 -production and attenuated salt-sensitive hypertension in DS rats.…”

Section: Loop Of Henlementioning

confidence: 99%

Oxidative Stress in Hypertension: Role of the Kidney

Araújo

Wilcox

2014

Antioxidants & Redox Signaling

152

131

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Significance: Renal oxidative stress can be a cause, a consequence, or more often a potentiating factor for hypertension. Increased reactive oxygen species (ROS) in the kidney have been reported in multiple models of hypertension and related to renal vasoconstriction and alterations of renal function. Nicotinamide adenine dinucleotide phosphate oxidase is the central source of ROS in the hypertensive kidney, but a defective antioxidant system also can contribute. Recent Advances: Superoxide has been identified as the principal ROS implicated for vascular and tubular dysfunction, but hydrogen peroxide (H 2 O 2 ) has been implicated in diminishing preglomerular vascular reactivity, and promoting medullary blood flow and pressure natriuresis in hypertensive animals. Critical Issues and Future Directions: Increased renal ROS have been implicated in renal vasoconstriction, renin release, activation of renal afferent nerves, augmented contraction, and myogenic responses of afferent arterioles, enhanced tubuloglomerular feedback, dysfunction of glomerular cells, and proteinuria. Inhibition of ROS with antioxidants, superoxide dismutase mimetics, or blockers of the reninangiotensin-aldosterone system or genetic deletion of one of the components of the signaling cascade often attenuates or delays the onset of hypertension and preserves the renal structure and function. Novel approaches are required to dampen the renal oxidative stress pathways to reduced O 2 -rather than H 2 O 2 selectivity and/or to enhance the endogenous antioxidant pathways to susceptible subjects to prevent the development and renaldamaging effects of hypertension. Antioxid. Redox Signal. 20, 74-101.

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“…Na ϩ Flux-In RPTs, increases in oxidative stress stimulate RPT sodium reabsorption by inhibition of basolateral Na/K-ATPase and apical NHE3 (27)(28)(29). We used GO-induced H 2 O 2 to examine if ouabain-induced ROS affects Na/K-ATPase signaling.…”

mentioning

confidence: 99%