The Role of NAD+ and NAD+-Boosting Therapies in Inflammatory Response by IL-13

The essential role of nicotinamide adenine dinucleotide+ (NAD+) in redox reactions during oxidative respiration is well known, yet the coenzyme and regulator functions of NAD+ in diverse and important processes are still being discovered. Maintaining NAD+ levels through diet is essential for health. In fact, the United States requires supplementation of the NAD+ precursor niacin into the food chain for these reasons. A large body of research also indicates that elevating NAD+ levels is beneficial for numerous conditions, including cancer, cardiovascular health, inflammatory response, and longevity. Consequently, strategies have been created to elevate NAD+ levels through dietary supplementation with NAD+ precursor compounds. This paper explores current research regarding these therapeutic compounds. It then focuses on the NAD+ 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+ 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+ and their associations with IL-13 signaling in the context of offering a means for safely and effectively reducing inflammatory response by IL-13.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:17

Enthalten in:

Pharmaceuticals (Basel, Switzerland) - 17(2024), 2 vom: 08. Feb.

Sprache:

Englisch

Beteiligte Personen:

Pugel, Anton D [VerfasserIn]
Schoenfeld, Alyssa M [VerfasserIn]
Alsaifi, Sara Z [VerfasserIn]
Holmes, Jocelyn R [VerfasserIn]
Morrison, Brad E [VerfasserIn]

Links:

Volltext

Themen:

Allergies
IL-13
Journal Article
NAD+
Nicotinamide mononucleotide
Nicotinamide riboside
Review

Anmerkungen:

Date Revised 27.02.2024

published: Electronic

Citation Status PubMed-not-MEDLINE

doi:

10.3390/ph17020226

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM368894266