Next Article in Journal
Perspectives for Ezrin and Radixin in Astrocytes: Kinases, Functions and Pathology
Next Article in Special Issue
Preeclampsia: Maternal Systemic Vascular Disorder Caused by Generalized Endothelial Dysfunction Due to Placental Antiangiogenic Factors
Previous Article in Journal
Recent Advances in Coarse-Grained Models for Biomolecules and Their Applications
Previous Article in Special Issue
Novel Biomarkers of Early Atherosclerotic Changes for Personalised Prevention of Cardiovascular Disease in Cervical Cancer and Human Papillomavirus Infection
Open AccessReview

Endothelial Dysfunction: Is There a Hyperglycemia-Induced Imbalance of NOX and NOS?

1
Department of Nutrition, Food & Exercise Sciences, Florida State University, Tallahassee, FL 32306, USA
2
Institute of Sports Sciences and Medicine, College of Human Sciences, Florida State University, Tallahassee, FL 32306, USA
3
Department of Biokinetics, Exercise and Leisure Sciences, School of Health Sciences, University of KwaZulu-Natal, Westville 4041, South Africa
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(15), 3775; https://doi.org/10.3390/ijms20153775
Received: 9 July 2019 / Revised: 29 July 2019 / Accepted: 31 July 2019 / Published: 2 August 2019
(This article belongs to the Special Issue Endothelial Dysfunction: Pathophysiology and Molecular Mechanisms)
NADPH oxidases (NOX) are enzyme complexes that have received much attention as key molecules in the development of vascular dysfunction. NOX have the primary function of generating reactive oxygen species (ROS), and are considered the main source of ROS production in endothelial cells. The endothelium is a thin monolayer that lines the inner surface of blood vessels, acting as a secretory organ to maintain homeostasis of blood flow. The enzymatic production of nitric oxide (NO) by endothelial NO synthase (eNOS) is critical in mediating endothelial function, and oxidative stress can cause dysregulation of eNOS and endothelial dysfunction. Insulin is a stimulus for increases in blood flow and endothelium-dependent vasodilation. However, cardiovascular disease and type 2 diabetes are characterized by poor control of the endothelial cell redox environment, with a shift toward overproduction of ROS by NOX. Studies in models of type 2 diabetes demonstrate that aberrant NOX activation contributes to uncoupling of eNOS and endothelial dysfunction. It is well-established that endothelial dysfunction precedes the onset of cardiovascular disease, therefore NOX are important molecular links between type 2 diabetes and vascular complications. The aim of the current review is to describe the normal, healthy physiological mechanisms involved in endothelial function, and highlight the central role of NOX in mediating endothelial dysfunction when glucose homeostasis is impaired. View Full-Text
Keywords: endothelium; eNOS; glucose; hyperglycemia; insulin resistance; NADPH oxidase; obesity; reactive oxygen species; ROS; type 2 diabetes; vascular function endothelium; eNOS; glucose; hyperglycemia; insulin resistance; NADPH oxidase; obesity; reactive oxygen species; ROS; type 2 diabetes; vascular function
Show Figures

Graphical abstract

MDPI and ACS Style

Meza, C.A.; La Favor, J.D.; Kim, D.-H.; Hickner, R.C. Endothelial Dysfunction: Is There a Hyperglycemia-Induced Imbalance of NOX and NOS? Int. J. Mol. Sci. 2019, 20, 3775.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop