ArticleAmerican journal of physiology. Renal physiology2016
Role of Nox4 and p67phox subunit of Nox2 in ROS production in response to increased tubular flow in the mTAL of Dahl salt-sensitive rats.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 33 citations in OpenAlex.
- Null mutation of the p67phox subunit of NOX2 permits compensatory changes in renal blood flow during the development of salt-sensitive hypertension in SS rats.American journal of physiology. Renal physiology · 2025Article
- Impact of Hematopoietic CD14 on Oxidative Stress during Salt-Sensitive Hypertension and Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Chromatin State Maps of Blood Pressure-Relevant Renal Segments Reveal Potential Regulatory Role for SNPs.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Effects of ROS pathway inhibitors and NADH and FADHArchives of biochemistry and biophysics · 2023Article
- Brown-Norway chromosome 1 mitigates the upregulation of proinflammatory pathways in mTAL cells and subsequent age-related CKD in Dahl SS/JrHsdMcwi rats.American journal of physiology. Renal physiology · 2023Article
- Metabolic Responses of Normal Rat Kidneys to a High Salt Intake.Function (Oxford, England) · 2023Article
- Fluid shear stress triggers cholesterol biosynthesis and uptake in inner medullary collecting duct cells, independently of nephrocystin-1 and nephrocystin-4.Frontiers in molecular biosciences · 2023Article
- Effect of Cardiotonic Steroid Marinobufagenin on Vascular Remodeling and Cognitive Impairment in Young Dahl-S Rats.International journal of molecular sciences · 2022Article
- Hydrogen peroxide (HScientific reports · 2021Article
- Genetic susceptibility of hypertension-induced kidney disease.Physiological reports · 2021Review
- DNA Methylation Sustains "Inflamed" Memory of Peripheral Immune Cells Aggravating Kidney Inflammatory Response in Chronic Kidney Disease.Frontiers in physiology · 2021Review
- NOX4-dependent regulation of ENaC in hypertension and diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Mechanistic computational modeling of the kinetics and regulation of NADPH oxidase 2 assembly and activation facilitating superoxide production.Free radical research · 2020Article
- Rat models of human diseases and related phenotypes: a systematic inventory of the causative genes.Journal of biomedical science · 2020Review
- NOX4/HHypertension (Dallas, Tex. : 1979) · 2020Article
- Sensing of tubular flow and renal electrolyte transport.Nature reviews. Nephrology · 2020Review
- Epigenetic Modifications in T Cells: The Role of DNA Methylation in Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Stretch-Induced Increases in Intracellular Ca Stimulate Thick Ascending Limb OHypertension (Dallas, Tex. : 1979) · 2020Article
- Voltage gated proton channels modulate mitochondrial reactive oxygen species production by complex I in renal medullary thick ascending limb.Redox biology · 2019Article
- Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019Review
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3 authors at 1 institution in 1 country.
Funding
Abstract
Nox4 and Nox2 are the most abundant NADPH oxidases (Nox) in the kidney and have been shown to contribute to hypertension, renal oxidative stress, and injury in Dahl salt-sensitive (SS) hypertensive rats. The present study focused on the role of Nox4 and p67phox/Nox2 in the generation of H2O2 and O2 (·-) in the renal medullary thick ascending limb of Henle (mTAL) of SS rats in response to increasing luminal flow (from 5 to 20 nl/min). Nox4 and p67phox/Nox2 genes were found to be expressed in the mTAL of SS rats. Responses of SS rats were compared with those of SS rats with knockout of Nox4 (SS(Nox4-/-)) or functional mutation of p67phox (SS(p67phox-/-)). Nox4 was the dominant source of increased intracellular H2O2 production in response to increased luminal flow as determined using the fluorescent dye peroxyfluor 6-AM (PF6-AM). The rate of mitochondrial H2O2 production [as determined by mitochondria peroxy yellow 1 (mitoPY1)] was also significantly reduced in SS(Nox4-/-) compared with SS rats, but not in SS(p67phox-/-) rats. In contrast, intracellular superoxide (O2 (·-)) production (the ratio of ethidium to dihydroethidium) in the mTAL of SS(Nox4-/-) rats was nearly identical to that of SS rats in response to luminal flow, indicating that Nox4 made no measurable contribution. mTAL O2 (·-) production was reduced in SS(p67phox-/-) compared with SS rats at the lower luminal flow of 5 nl/min and progressively increased when perfusion was changed to 20 nl/min. We conclude that increased mTAL luminal flow results in increases in intracellular and mitochondrial H2O2, which are dependent on the presence of Nox4, and that p67phox/Nox2 accounts solely for increases in O2 (·-) production.
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