The Role of NAD<sup>+</sup> and NAD<sup>+</sup>-Boosting Therapies in Inflammatory Response by IL-13

The essential role of nicotinamide adenine dinucleotide<sup>+</sup> (NAD<sup>+</sup>) in redox reactions during oxidative respiration is well known, yet the coenzyme and regulator functions of NAD<sup>+</sup> in diverse and important processes are still being disc...

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Bibliographic Details
Main Authors: Anton D. Pugel, Alyssa M. Schoenfeld, Sara Z. Alsaifi, Jocelyn R. Holmes, Brad E. Morrison
Format: Article
Language:English
Published: MDPI AG 2024-02-01
Series:Pharmaceuticals
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Online Access:https://www.mdpi.com/1424-8247/17/2/226
Description
Summary:The essential role of nicotinamide adenine dinucleotide<sup>+</sup> (NAD<sup>+</sup>) in redox reactions during oxidative respiration is well known, yet the coenzyme and regulator functions of NAD<sup>+</sup> in diverse and important processes are still being discovered. Maintaining NAD<sup>+</sup> levels through diet is essential for health. In fact, the United States requires supplementation of the NAD<sup>+</sup> precursor niacin into the food chain for these reasons. A large body of research also indicates that elevating NAD<sup>+</sup> levels is beneficial for numerous conditions, including cancer, cardiovascular health, inflammatory response, and longevity. Consequently, strategies have been created to elevate NAD<sup>+</sup> levels through dietary supplementation with NAD<sup>+</sup> precursor compounds. This paper explores current research regarding these therapeutic compounds. It then focuses on the NAD<sup>+</sup> regulation of IL-13 signaling, which is a research area garnering little attention. IL-13 is a critical regulator of allergic response and is associated with Parkinson’s disease and cancer. Evidence supporting the notion that increasing NAD<sup>+</sup> levels might reduce IL-13 signal-induced inflammatory response is presented. The assessment is concluded with an examination of reports involving popular precursor compounds that boost NAD<sup>+</sup> and their associations with IL-13 signaling in the context of offering a means for safely and effectively reducing inflammatory response by IL-13.
ISSN:1424-8247