ArticleCNS neuroscience & therapeutics2014
Extracellular visfatin has nicotinamide phosphoribosyltransferase enzymatic activity and is neuroprotective against ischemic injury.
Article in CNS neuroscience & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 64 citations in OpenAlex.
- Adipocytokines as Pathogenic Mediators and Therapeutic Targets in Metabolic Syndrome-Related Cardiocerebrovascular Events.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- The obesity paradox in cognitive decline: Impact of BMI dynamics and APOE genotypes across various cognitive status.Diabetes, obesity & metabolism · 2025Article
- Extracellular nicotinamide phosphoribosyltransferase (eNAMPT) drives abnormal pericyte-rich vasculature in triple-negative breast cancer.Angiogenesis · 2024Article
- Targeting Adipokines: A Promising Therapeutic Strategy for Epilepsy.Neurochemical research · 2024Review
- Inflammatory lung injury is associated with endothelial cell mitochondrial fission and requires the nitration of RhoA and cytoskeletal remodeling.Free radical biology & medicine · 2024Article
- Article
- The Role of Adipokines in the Pathologies of the Central Nervous System.International journal of molecular sciences · 2023Review
- Notoginseng leaf triterpenes ameliorates mitochondrial oxidative injury via the NAMPT-SIRT1/2/3 signaling pathways in cerebral ischemic model rats.Journal of ginseng research · 2023Article
- Protective effects of Gypenoside XVII against cerebral ischemia/reperfusion injury via SIRT1-FOXO3A- and Hif1a-BNIP3-mediated mitochondrial autophagy.Journal of translational medicine · 2022Article
- Astrocyte-derived exosomal nicotinamide phosphoribosyltransferase (Nampt) ameliorates ischemic stroke injury by targeting AMPK/mTOR signaling to induce autophagy.Cell death & disease · 2022Article
- Allisartan isoproxil reduces mortality of stroke-prone rats and protects against cerebrovascular, cardiac, and aortic damage.Acta pharmacologica Sinica · 2021Article
- Dysregulation of Insulin-Linked Metabolic Pathways in Alzheimer's Disease: Co-Factor Role of Apolipoprotein EJournal of Alzheimer's disease reports · 2020Article
- Notoginseng Leaf Triterpenes Ameliorates OGD/R-Induced Neuronal Injury via SIRT1/2/3-Foxo3a-MnSOD/PGC-1Oxidative medicine and cellular longevity · 2020Article
- Nicotinamide Mononucleotide: A Promising Molecule for Therapy of Diverse Diseases by Targeting NAD+ Metabolism.Frontiers in cell and developmental biology · 2020Review
- NAMPT and BMAL1 Are Independently Involved in the Palmitate-Mediated Induction of Neuroinflammation in Hypothalamic Neurons.Frontiers in endocrinology · 2020Article
- Intracerebroventricular Delivery of Recombinant NAMPT Deters Inflammation and Protects Against Cerebral Ischemia.Translational stroke research · 2019Article
- The Novel Perspectives of Adipokines on Brain Health.International journal of molecular sciences · 2019Review
- Subcellular compartmentalization of NADPharmacology & therapeutics · 2019Review
- Targeting NAMPT as a therapeutic strategy against stroke.Stroke and vascular neurology · 2019Review
- Mitochondrial complex I deficiency and cardiovascular diseases: current evidence and future directions.Journal of molecular medicine (Berlin, Germany) · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimVisfatin, a novel adipokine, is predominantly produced by visceral adipose tissue and exists in intracellular and extracellular compartments. The intracellular form of visfatin is proved to be nicotinamide phosphoribosyltransferase (NAMPT) and exhibits neuroprotection through maintaining intracellular NAD(+) pool. However, whether extracellular form of visfatin has NAMPT activity and the effect of extracellular visfatin in cerebral ischemia are unknown. METHODS AND
resultsPlasma concentrations of visfatin, NAD(+) , and ATP were increased in mice upon cerebral ischemia. Cultured glia, but not neuron, was able to secrete visfatin. Oxygen-glucose deprivation (OGD) stress increased the secretion of visfatin from glia. Extracellular recombinant mouse wild-type visfatin, but not mouse H247A-mutant enzymatic-dead visfatin, had NAMPT enzymatic function in vitro. Treatment of wild-type visfatin, but not H247A-mutant enzymatic-dead visfatin, significantly attenuated detrimental effect of OGD on the cell viability and apoptosis in both cultured mouse neuron and glia. Treatment of neutralizing antibody, abolished the protective effect of extracellular visfatin on cell viability, but failed to block the antiapoptotic effect of extracellular visfatin. At last, we observed that plasma visfatin concentrations decreased in 6-month-old but not 3-month-old SHR-SP compared with that in age-matched Wistar-Kyoto rats. Inhibition of NAMPT enzymatic function of visfatin (by FK866) accelerated the occurrence of stroke in SHR-SP.
conclusionsExtracellular visfatin has NAMPT enzymatic activity and maybe be neuroprotective just as intracellular visfatin in cerebral ischemic injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.