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. 2021 Apr 24;9(4):959–972. doi: 10.1016/j.gendis.2021.04.001

Figure 2.

Fig. 2

Nicotinamide adenine dinucleotide (NAD+) exerts beneficial effects on CVDs by regulating metabolism, maintaining redox homeostasis and modulating immune responses. The NAD+ coenzyme is reduced to NADH during glycolysis, fatty acid β-oxidation and the tricarboxylic acid (TCA) cycle. NAD+ can regulate mitochondrial biogenesis through the SIRT1/PGC1α pathway and enhance autophagy through the SIRT1/AMPK/HIF pathway. These effects of NAD+ in metabolism contribute to its invention potential for CVDs treatment. The balance of NAD+ and NADH is a key component of the redox state of a cell. NAD+ can exert antioxidant effects by activating SIRTs to regulate FOXOs, NRF2, SOD and GSH, thus countering oxidative stress in CVDs. NAD+ can also suppress the central immune pathway and regulate T-cell homeostasis to exert immunomodulatory effects, which might be beneficial as a treatment of CVDs. AMPK, adenosine monophosphate-activated protein kinase; CVDs, cardiovascular diseases; FOXOs, class O of forkhead box family; GSH, glutathione; HIF, hypoxia inducible factors; NRF2, nuclear factor E2-related factor 2; PGC1α, peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1α; ROS, reactive oxygen species; SOD, superoxide dismutase.