Therapeutic correlation of NOX4 and diabetes-mediated neurodegeneration

Abstract

The NOX family consists of seven isoenzymes that produce reactive oxygen species (ROS) from molecular oxygen. Changes in redox balance may impact disorders linked to metabolic dysfunction, as enzymes and a subcellular compartment that generally produce ROS are connected to metabolic control. A condition known as diabetes affects how the body distributes and processes macronutrients, including proteins, lipids, and carbohydrates. ROS plays a crucial role because individuals with neurodegenerative illnesses frequently have high levels of oxidative stress in their brains. While many ROS are intracellular signaling messengers and most oxidative metabolism products are beneficial to normal cellular function, increased ROS levels caused by hyperglycemia, peroxisomes, and certain enzymes cause oxidative stress-sensitive signaling, toxicity, neurodegenerative diseases, and diabetes. NADPH oxidase 4 (NOX4) is a protein expressed throughout the body and in different cells and areas of the brain. There is emerging proof that several neurodegenerative conditions can increase isoform NOX4 expression. Pharmacological suppression of NOX4 enzymes is neuroprotective and can lessen harmful elements of disease after Parkinson's, Alzheimer's, stroke, ataxia, multiple system atrophy, and peripheral neuropathy, as well as in diabetes disorders. This review investigates pharmacological strategies for targeting this important oxidative stress system, explores the findings suggesting NOX4 participation in the pathophysiology of several neurological illnesses, and lists barriers to getting these treatments into the clinic. We have also discussed the prospect of transcriptional alterations concerning NOX as a molecular link between neurodegenerative disease (NDD) and diabetes.