NMN protects vascular endothelial cells from M1 macrophage-derived IL-1β-induced hyperpermeability by inhibiting VE-cadherin degradation - Scorecard - MDSpire

NMN protects vascular endothelial cells from M1 macrophage-derived IL-1β-induced hyperpermeability by inhibiting VE-cadherin degradation

  • By

  • Takeshi Katayoshi

  • Takahisa Nakajo

  • Natsuko Kitajima

  • Wakana Naka

  • Yuki Kamei

  • Taiki Fushimi

  • Masakatsu Kageyama

  • Mitsugu Akagawa

  • Kentaro Tsuji

  • May 18, 2026

  • 0 min

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Clinical Scorecard: Nicotinamide Mononucleotide Safeguards Endothelial Cells from IL-1β-Induced Hyperpermeability by Preventing VE-Cadherin Degradation Triggered by M1 Macrophages

At a Glance

CategoryDetail
Condition
Key MechanismsNMN prevents IL-1β-induced NF-κB activation and VE-cadherin degradation, emphasizing the NAD+-SIRT1 axis.
Target Population
Care Setting

Key Highlights

  • NMN attenuates hyperpermeability induced by M1 macrophages
  • IL-1β is a primary contributor to endothelial hyperpermeability
  • NMN's protective effect is dependent on the NAD+-SIRT1 axis
  • VE-cadherin is crucial for maintaining endothelial barrier integrity
  • Other NAD+ precursors also protect against IL-1β-induced effects

Guideline-Based Recommendations

Diagnosis

    Management

    • C
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    Monitoring & Follow-up

      Risks

        Patient & Prescribing Data

        Include specific dosing recommendations for NMN supplementation.

        Clinical Best Practices

        • monitoring

        Related Resources & Content

        Original Source(s)

        NMN protects vascular endothelial cells from M1 macrophage-derived IL-1β-induced hyperpermeability by inhibiting VE-cadherin degradation

        • by Takeshi Katayoshi, Takahisa Nakajo, Natsuko Kitajima, Wakana Naka, Yuki Kamei, Taiki Fushimi, Masakatsu Kageyama, Mitsugu Akagawa, Kentaro Tsuji

        • May 18, 2026

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