Authors
Panshen Xu, Weilong Song, Hebin Pan, Jialong Yang, Jiapeng Deng, An Wang, Kaitao Wang, Dingsheng Lin
Published in
Archives of pharmacal research. Oct 22, 2026. Epub Oct 22, 2026.
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.
PMID:
42907702
Bibliographic data and abstract were imported from PubMed on 23 Oct 2026.
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