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Study · In vitro (cells) · 2026

4 results

Intracellular NAD+ Depletion Increases Prostanoid Production via p38/COX2 Signalling in FK866-Induced Senescent Human Umbilical Vein Endothelial Cells.

Kitajima N, Nakajo T, Katayoshi T, Tsuji K

Journal of cellular and molecular medicine1 May 2026

PMID42159653 (opens in a new tab)PMCIDPMC13240423 (opens in a new tab)DOI10.1111/jcmm.71187 (opens in a new tab)PepBankPUB-42159653
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Summary

Vascular endothelial cells maintain vascular homeostasis by releasing mediators with vasoconstrictive and vasorelaxant effects. Prostanoids are bioactive substances synthesised by cyclooxygenase2 (COX2); they preserve vascular function and can increase the risk of cardiovascular disease (CVD) associated with ageing. Age-related reductions in nicotinamide adenine dinucleotide (NAD+) have been implicated in CVD pathogenesis. However, the relationship between intracellular NAD+ levels and prostanoid production in vascular endothelial cells is unclear. Herein, reduced intracellular NAD+ levels upregulated COX2 protein expression by activating the p38 mitogen-activated protein kinase (MAPK) signalling pathway, increasing the production of prostaglandin F1α (PGF1α) and thromboxane B2 (TXB2) in human umbilical vein endothelial cells (HUVECs). Treatment with the nicotinamide phosphoribosyltransferase (NAMPT) inhibitor, FK866, decreased intracellular NAD+ levels, induced a cellular senescence-like phenotype characterised by the suppression of cell proliferation without cell death and promoted PGF1α and TXB2 production in HUVECs. FK866 treatment increased phosphorylated p38 and COX2 protein levels, whereas treatment with the p38 inhibitor, PD169316, suppressed the FK866-induced increase in COX2 expression. Supplementation with nicotinamide mononucleotide (NMN), a precursor of NAD+, following FK866 treatment restored intracellular NAD+ levels, reduced the cellular senescence-like phenotype and attenuated the production of PGF1α and TXB2. These results suggest that intracellular NAD+ appears to regulate prostanoid production in HUVECs under conditions of acute depletion.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

4 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In FK866-treated HUVECs, NMN restored intracellular NAD levels.

    In plain wordsIn cells treated with FK866, NMN restored NAD levels inside the cells.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseIntracellular NAD
    Study

    humann: not reported in source

    FK866-treated HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with nicotinamide mononucleotide (NMN), a precursor of NAD+, following FK866 treatment restored intracellular NAD+ levels, reduced the cellular senescence-like phenotype and attenuated the production of PGF1α and TXB2.
  2. 02LabIn vitro (cells)Mechanism

    In FK866-treated HUVECs, NMN reduced the cellular senescence-like phenotype.

    In plain wordsIn cells treated with FK866, NMN reduced signs resembling cellular aging.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseSenescence-like phenotype
    Study

    humann: not reported in source

    FK866-treated HUVECs
    Outcome group
    Aging markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with nicotinamide mononucleotide (NMN), a precursor of NAD+, following FK866 treatment restored intracellular NAD+ levels, reduced the cellular senescence-like phenotype and attenuated the production of PGF1α and TXB2.
  3. 03LabIn vitro (cells)Mechanism

    In FK866-treated HUVECs, NMN attenuated PGF1α production.

    In plain wordsIn cells treated with FK866, NMN reduced PGF1α production.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreasePGF1α production
    Study

    humann: not reported in source

    FK866-treated HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with nicotinamide mononucleotide (NMN), a precursor of NAD+, following FK866 treatment restored intracellular NAD+ levels, reduced the cellular senescence-like phenotype and attenuated the production of PGF1α and TXB2.
  4. 04LabIn vitro (cells)Mechanism

    In FK866-treated HUVECs, NMN attenuated TXB2 production.

    In plain wordsIn cells treated with FK866, NMN reduced TXB2 production.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseTXB2 production
    Study

    humann: not reported in source

    FK866-treated HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with nicotinamide mononucleotide (NMN), a precursor of NAD+, following FK866 treatment restored intracellular NAD+ levels, reduced the cellular senescence-like phenotype and attenuated the production of PGF1α and TXB2.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

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