NADPH Oxidases in Metabolic Homeostasis

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (30 April 2019) | Viewed by 8419

Special Issue Editor


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Guest Editor
Service of Endocrinology, Diabetology, Nutrition and Patient Education Department of Internal Medicine, Geneva University Hospitals and University of Geneva,1211 Geneva, Switzerland
Interests: diabetes, NADPH oxidase enzymes, reactive oxygen species, oxidative stress, fatty liver disease, islet cells, adipose tissue, metabolism
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Special Issue Information

Dear Colleagues,

Metabolic homeostasis is maintained by a tightly regulated balance between energy intake, storage, and utilization. Chronic energy balance surplus results in obesity, leading to the onset of insulin resistance, diabetes, and a variety of metabolic complications. Formerly, the development of these metabolic disturbances was considered to be linked to the production of reactive oxygen species (ROS), inevitably associated with the onset of oxidative stress. Currently, however, the role of ROS is regarded in a more refined fashion. Indeed, ROS produced in physiological quantities, in a timely and spatially regulated manner, are acknowledged as critical physiological regulators of diverse metabolic processes and cellular functions. NADPH oxidases (NOX-es) and dual oxidases (DUOX-es) belong to a family of enzymes with the primary function of ROS production. NOX/DUOX isoforms are present in tissues with prominent roles in the regulation of metabolic homeostasis (e.g., liver, muscle, kidney, white and brown adipose tissues, the hypothalamus, and the islets of the pancreas). In several of these tissues, dysregulated NOX/DUOX expression or activation has been associated with disturbed insulin signaling and metabolic function. Due to their tightly-controlled ROS production, NOX/DUOX enzymes elicit high interest in relation to both metabolic health sustainment and the development of metabolic disorders, and are thus considered to be promising pharmaceutical targets in obesity, insulin resistance, and diabetes.

The aim of this “Special Issue” is to provide a forum for recent research advances regarding the regulatory function of NOX/DUOX isoforms in the maintenance of metabolic balance and their alterations in diabetes and diabetes-related complications.

Dr. Ildiko Szanto
Guest Editor

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Published Papers (1 paper)

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Review

21 pages, 1999 KiB  
Review
H2O2 Metabolism in Normal Thyroid Cells and in Thyroid Tumorigenesis: Focus on NADPH Oxidases
by Ildiko Szanto, Marc Pusztaszeri and Maria Mavromati
Antioxidants 2019, 8(5), 126; https://doi.org/10.3390/antiox8050126 - 10 May 2019
Cited by 41 | Viewed by 8070
Abstract
Thyroid hormone synthesis requires adequate hydrogen peroxide (H2O2) production that is utilized as an oxidative agent during the synthesis of thyroxin (T4) and triiodothyronine (T3). Thyroid H2O2 is generated by a member of the family of [...] Read more.
Thyroid hormone synthesis requires adequate hydrogen peroxide (H2O2) production that is utilized as an oxidative agent during the synthesis of thyroxin (T4) and triiodothyronine (T3). Thyroid H2O2 is generated by a member of the family of NADPH oxidase enzymes (NOX-es), termed dual oxidase 2 (DUOX2). NOX/DUOX enzymes produce reactive oxygen species (ROS) as their unique enzymatic activity in a timely and spatially regulated manner and therefore, are important regulators of diverse physiological processes. By contrast, dysfunctional NOX/DUOX-derived ROS production is associated with pathological conditions. Inappropriate DUOX2-generated H2O2 production results in thyroid hypofunction in rodent models. Recent studies also indicate that ROS improperly released by NOX4, another member of the NOX family, are involved in thyroid carcinogenesis. This review focuses on the current knowledge concerning the redox regulation of thyroid hormonogenesis and cancer development with a specific emphasis on the NOX and DUOX enzymes in these processes. Full article
(This article belongs to the Special Issue NADPH Oxidases in Metabolic Homeostasis)
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