The emerging role of NADPH oxidase NOX5 in vascular disease

Jay C. Jha, Anna M. D. Watson, Geetha Mathew, Lisanne C. de Vos, Karin Jandeleit-Dahm

Research output: Contribution to journalEditorialOtherpeer-review

18 Citations (Scopus)

Abstract

Oxidative stress is a consequence of up-regulation of pro-oxidant enzyme-induced reactive oxygen species (ROS) production and concomitant depletion of antioxidants. Elevated levels of ROS act as an intermediate and are the common denominator for various diseases including diabetes-associated macro-/micro-vascular complications and hypertension. A range of enzymes are capable of generating ROS, but the pro-oxidant enzyme family, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs), are the only enzymes known to be solely dedicated to ROS generation in the vascular tissues, kidney, aortas and eyes. While there is convincing evidence for a role of NOX1 in vascular and eye disease and for NOX4 in renal injury, the role of NOX5 in disease is less clear. Although NOX5 is highly up-regulated in humans in disease, it is absent in rodents. Thus, so far it has not been possible to study NOX5 in traditional mouse or rat models of disease. In the present review, we summarize and critically analyse the emerging evidence for a pathophysiological role of NOX5 in disease including the expression, regulation and molecular and cellular mechanisms which have been demonstrated to be involved in NOX5 activation.

Original languageEnglish
Pages (from-to)981-990
Number of pages10
JournalClinical Science
Volume131
Issue number10
DOIs
Publication statusPublished - 2017

Cite this

@article{4632a79a87f84b9fad96f2da1460b3c4,
title = "The emerging role of NADPH oxidase NOX5 in vascular disease",
abstract = "Oxidative stress is a consequence of up-regulation of pro-oxidant enzyme-induced reactive oxygen species (ROS) production and concomitant depletion of antioxidants. Elevated levels of ROS act as an intermediate and are the common denominator for various diseases including diabetes-associated macro-/micro-vascular complications and hypertension. A range of enzymes are capable of generating ROS, but the pro-oxidant enzyme family, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs), are the only enzymes known to be solely dedicated to ROS generation in the vascular tissues, kidney, aortas and eyes. While there is convincing evidence for a role of NOX1 in vascular and eye disease and for NOX4 in renal injury, the role of NOX5 in disease is less clear. Although NOX5 is highly up-regulated in humans in disease, it is absent in rodents. Thus, so far it has not been possible to study NOX5 in traditional mouse or rat models of disease. In the present review, we summarize and critically analyse the emerging evidence for a pathophysiological role of NOX5 in disease including the expression, regulation and molecular and cellular mechanisms which have been demonstrated to be involved in NOX5 activation.",
author = "Jha, {Jay C.} and Watson, {Anna M. D.} and Geetha Mathew and {de Vos}, {Lisanne C.} and Karin Jandeleit-Dahm",
year = "2017",
doi = "10.1042/CS20160846",
language = "English",
volume = "131",
pages = "981--990",
journal = "Clinical Science and Molecular Medicine",
issn = "0009-9287",
publisher = "Portland Press",
number = "10",

}

The emerging role of NADPH oxidase NOX5 in vascular disease. / Jha, Jay C.; Watson, Anna M. D.; Mathew, Geetha; de Vos, Lisanne C.; Jandeleit-Dahm, Karin.

In: Clinical Science, Vol. 131, No. 10, 2017, p. 981-990.

Research output: Contribution to journalEditorialOtherpeer-review

TY - JOUR

T1 - The emerging role of NADPH oxidase NOX5 in vascular disease

AU - Jha, Jay C.

AU - Watson, Anna M. D.

AU - Mathew, Geetha

AU - de Vos, Lisanne C.

AU - Jandeleit-Dahm, Karin

PY - 2017

Y1 - 2017

N2 - Oxidative stress is a consequence of up-regulation of pro-oxidant enzyme-induced reactive oxygen species (ROS) production and concomitant depletion of antioxidants. Elevated levels of ROS act as an intermediate and are the common denominator for various diseases including diabetes-associated macro-/micro-vascular complications and hypertension. A range of enzymes are capable of generating ROS, but the pro-oxidant enzyme family, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs), are the only enzymes known to be solely dedicated to ROS generation in the vascular tissues, kidney, aortas and eyes. While there is convincing evidence for a role of NOX1 in vascular and eye disease and for NOX4 in renal injury, the role of NOX5 in disease is less clear. Although NOX5 is highly up-regulated in humans in disease, it is absent in rodents. Thus, so far it has not been possible to study NOX5 in traditional mouse or rat models of disease. In the present review, we summarize and critically analyse the emerging evidence for a pathophysiological role of NOX5 in disease including the expression, regulation and molecular and cellular mechanisms which have been demonstrated to be involved in NOX5 activation.

AB - Oxidative stress is a consequence of up-regulation of pro-oxidant enzyme-induced reactive oxygen species (ROS) production and concomitant depletion of antioxidants. Elevated levels of ROS act as an intermediate and are the common denominator for various diseases including diabetes-associated macro-/micro-vascular complications and hypertension. A range of enzymes are capable of generating ROS, but the pro-oxidant enzyme family, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs), are the only enzymes known to be solely dedicated to ROS generation in the vascular tissues, kidney, aortas and eyes. While there is convincing evidence for a role of NOX1 in vascular and eye disease and for NOX4 in renal injury, the role of NOX5 in disease is less clear. Although NOX5 is highly up-regulated in humans in disease, it is absent in rodents. Thus, so far it has not been possible to study NOX5 in traditional mouse or rat models of disease. In the present review, we summarize and critically analyse the emerging evidence for a pathophysiological role of NOX5 in disease including the expression, regulation and molecular and cellular mechanisms which have been demonstrated to be involved in NOX5 activation.

UR - http://www.scopus.com/inward/record.url?scp=85018374394&partnerID=8YFLogxK

U2 - 10.1042/CS20160846

DO - 10.1042/CS20160846

M3 - Editorial

VL - 131

SP - 981

EP - 990

JO - Clinical Science and Molecular Medicine

JF - Clinical Science and Molecular Medicine

SN - 0009-9287

IS - 10

ER -