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NMRK2-YAP-NADK axis preserves redox protection against myocardial ischemia/reperfusion injury

Chao Zhang1, Jie Wang2, Jing Chi3

  • 1Department of Anesthesiology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China; Department of Anesthesiology, Suzhou Ninth Hospital Affiliated to Soochow University, Suzhou, Jiangsu, China; Institute of Anesthesiology, Soochow University, Suzhou, Jiangsu, China.

Redox Biology
|February 28, 2026
PubMed

Insights

Nicotinamide riboside kinase 2 (NMRK2) protects the heart from oxidative stress by boosting antioxidant capacity. This novel redox therapy involves NMRK2 disrupting the integrin β-YAP complex, enhancing NAD kinase transcription for myocardial ischemia/reperfusion injury.

Area of Science:

  • Cardiovascular Biology
  • Redox Biology
  • Molecular Medicine

Background:

  • Myocardial ischemia/reperfusion (I/R) injury causes significant oxidative stress, leading to cell death and heart failure.
  • Effective redox therapies for I/R injury are limited, highlighting a critical unmet clinical need.

Purpose of the Study:

  • To investigate the role of nicotinamide riboside kinase 2 (NMRK2) in myocardial I/R injury.
  • To elucidate the novel redox-protective mechanism of NMRK2.

Main Methods:

  • Established mouse models of myocardial I/R and cardiomyocyte hypoxia/reoxygenation (H/R) injury.
  • Utilized gene overexpression and knockdown (NMRK2, NAD kinase, integrin β), cell fractionation, co-immunoprecipitation, and ChIP-qPCR assays.
  • Assessed cellular antioxidant capacity by measuring NADPH, NAD+/NADH, GSH/GSSG ratios, and Trx1 activation.

Main Results:

  • NMRK2 overexpression enhanced cellular antioxidant capacity and reduced oxidative damage in I/R and H/R injury models.
  • NMRK2 promoted nuclear entry of Yes-associated protein (YAP) by disrupting the integrin β-YAP interaction.
  • YAP directly activated NAD kinase (NADK) transcription, which was essential for NMRK2's protective effects.

Conclusions:

  • NMRK2 provides redox protection against myocardial I/R injury through a novel mechanism involving YAP.
  • NMRK2 disrupts the integrin β-YAP complex, leading to YAP-dependent NADK transcription and enhanced antioxidant capacity.
  • NMRK2 represents a promising, translatable therapeutic strategy for myocardial I/R injury.
Keywords:
CardiomyocytesMyocardial ischemia-reperfusion injuryNADKNMRK2Redox protectionYAP

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