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Related Experiment Video

Updated: Jun 23, 2026

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
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Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation

Published on: January 10, 2025

NUAK1 Inhibition Alleviates Ischemia-Reperfusion Injury via SYNE1-YAP1.

Yangjinming Bai1, Tingting Zhao1, Qian Wang1

  • 1Department of Cardiology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China.

Circulation Research
|June 22, 2026
PubMed
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NUAK1 (AMPK-related kinase 5) regulates SYNE1 (Nesprin-1) phosphorylation, controlling YAP1 (Yes-associated protein 1) nuclear entry. Inhibiting NUAK1 reduces heart injury during ischemia-reperfusion by enhancing YAP1 activity.

Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanotransduction
  • Molecular Signaling

Background:

  • Mechanosensitive nuclear signaling plays a role in myocardial ischemia-reperfusion injury.
  • The specific substrates and mechanisms involving NUAK1 (AMPK-related kinase 5) in this process are not fully understood.

Purpose of the Study:

  • To investigate if NUAK1 regulates the SYNE1 (Nesprin-1)/cytoskeleton-dependent nuclear gating of YAP1 (Yes-associated protein 1) during cellular stress.
  • To elucidate the role of the NUAK1-SYNE1 axis in myocardial ischemia-reperfusion injury.

Main Methods:

  • Quantitative phosphoproteomics to identify NUAK1 phosphorylation sites on SYNE1.
  • Coimmunoprecipitation and in vitro kinase assays to confirm direct phosphorylation.
  • Genetic and pharmacological inhibition of NUAK1 in neonatal mouse ventricular myocytes and a mouse model of ischemia-reperfusion injury.
Keywords:
animalscytoskeletonhypoxiamyocardial reperfusionnuclear matrix

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  • Atomic force microscopy to assess nuclear mechanical remodeling.

    • Main Results:

    • NUAK1 directly phosphorylates SYNE1 at a conserved site (S434).
    • NUAK1 inhibition in cardiomyocytes reduced apoptosis, decreased SYNE1 stability, and promoted YAP1 nuclear localization and activity.
    • The NUAK1-SYNE1 pathway restrains YAP1 nuclear accumulation under stress, influencing nuclear mechanical properties.
    • NUAK1 inhibition attenuated myocardial damage and improved remodeling in an in vivo injury model.

    Conclusions:

    • NUAK1-dependent SYNE1 phosphorylation is a key regulator of nuclear mechanosignaling during ischemic stress.
    • Downregulation of NUAK1 enhances cardiomyocyte YAP1 nuclear activity and mitigates injury responses, offering a potential therapeutic target.