ArticleArchives of pharmacal research2026
Nicotinamide riboside promotes skin flap survival by enhancing autophagy associated with the NAD⁺/SIRT1-FOXO1 signaling axis.
Article in Archives of pharmacal research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Flap transplantation is a widely used clinical approach for wound repair, organ reconstruction, and aesthetic restoration. However, ischemic flap necrosis remains a serious postoperative complication, driven by multiple factors, including inadequate blood perfusion, oxidative stress, and cell death. Nicotinamide riboside (NR), a bioavailable precursor of NAD⁺, can increase intracellular NAD⁺ levels following supplementation. This study aimed to investigate the protective effects of NR against ischemic flap injury. In vitro, NR attenuated oxygen-glucose deprivation/reperfusion (OGD/R)-induced injury in HUVECs. Co-immunoprecipitation (Co-IP) assays showed an association between sirtuin-1 (SIRT1) and forkhead box O1 (FOXO1). FOXO1 knockdown partially impaired NR-associated autophagic responses, whereas FOXO1 overexpression partially restored autophagic responses following SIRT1 silencing. NR supplementation increased intracellular NAD⁺ levels and enhanced autophagic activity in OGD/R-treated HUVECs, accompanied by changes in SIRT1, FOXO1, and Ac-FOXO1. In a rat model of ischemic skin flaps, NR administration improved flap survival and was accompanied by enhanced angiogenic responses, autophagy-associated changes, and reduced ferroptosis-related alterations. Collectively, these findings indicate that NR exerts protective effects against ischemic flap injury in rats and support the involvement of NAD⁺/SIRT1-FOXO1 signaling in NR-associated autophagic responses.
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