Nampt: a new therapeutic target for modulating NAD+ levels in metabolic, cardiovascular, and neurodegenerative diseases

Can J Physiol Pharmacol. 2025 Jul 1;103(7):208-224. doi: 10.1139/cjpp-2024-0400. Epub 2025 Apr 9.

Abstract

NAD+ is an important cofactor involved in regulating many biochemical processes in cells. An imbalance in NAD+/NADH ratio is linked to many diseases. NAD+ is depleted in diabetes, cardiovascular and neurodegenerative diseases, and in aging, and is increased in tumor cells. NAD+ is generated in cells via the de novo, Preiss-Handler, and salvage pathways. Most of the cellular NAD+ is generated through Nampt activation, a key rate-limiting enzyme that is involved in the salvage pathway. Restoration of NAD+/NADH balance offers therapeutic advantages for improving tissue homeostasis and function. NAD+ is known to benefit and restore the body's physiological mechanisms, including DNA replication, chromatin and epigenetic modifications, and gene expression. Recent studies elucidate the role of NAD+ in cells utilizing transgenic mouse models. Translational new therapeutics are positioned to utilize the NAD+ restoration strategies for overcoming the drawbacks that exist in the pharmacological toolkit. The present review highlights the significance of Nampt-NAD+ axis as a major player in energy metabolism and provides an overview with insights into future strategies, providing pharmacological advantages to address current and future medical needs.

Keywords: NAD+; Nampt; cardiovascular and neurodegenerative diseases; diabetes; skeletal muscle.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases* / drug therapy
  • Cardiovascular Diseases* / metabolism
  • Cytokines* / metabolism
  • Humans
  • Metabolic Diseases* / drug therapy
  • Metabolic Diseases* / metabolism
  • Molecular Targeted Therapy
  • NAD* / metabolism
  • Neurodegenerative Diseases* / drug therapy
  • Neurodegenerative Diseases* / metabolism
  • Nicotinamide Phosphoribosyltransferase* / antagonists & inhibitors
  • Nicotinamide Phosphoribosyltransferase* / metabolism

Substances

  • Nicotinamide Phosphoribosyltransferase
  • NAD
  • Cytokines
  • nicotinamide phosphoribosyltransferase, human