Fig. 4: Strategies to modulate NAD⁺ homeostasis in various contexts.

The figure summarizes several ways to control NAD⁺ and downstream effectors. These include: (1) Modulating NAD⁺ synthesis via activators or inhibitors of NAPRT, NAMPT, and amino-carboxy-muconate-semialdehyde decarboxylase (ACMSD); (2) Enhancing NAD⁺-dependent deacylation through sirtuins via compound interventions; (3) Compound-based inhibition of NAD⁺ consumption by targeting CD38, PARPs, NNMT, and SARM1. These approaches can yield benefits in diverse conditions such as metabolic disorders, inflammation, and neurological diseases. Frequently reported compounds and associated applications are indicated for each strategy. For more compounds studied across various health conditions, refer to the main text. CIPN chemotherapy-induced peripheral neuropathy, NAFLD non-alcoholic fatty liver disease. Created in BioRender. https://BioRender.com/0mrb07s.