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HSP90-Mediates Liraglutide Preconditioning-Induced Cardioprotection by Inhibiting C5a and NF-κB.

Shi-Tao He1, Dong-Xiao Wang1, Jian-Jun Meng2

  • 1Department of Cardiology, First Affiliated Hospital, Guangxi Medical University, Nanning, China.

Journal of Investigative Surgery : the Official Journal of the Academy of Surgical Research
|October 21, 2021
PubMed
Summary

Liraglutide preconditioning protects the heart by inhibiting complement C5a and NF-κB signaling via HSP90. This mechanism reduces inflammation and cardiomyocyte apoptosis, offering a novel therapeutic strategy for ischemic heart disease.

Keywords:
C5aHSP90Liraglutide preconditioningNF-κBinflammationischemia/reperfusion

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Immunology

Background:

  • Heat shock protein 90 (HSP90) is known to inhibit complement C5a, contributing to cardioprotection.
  • Liraglutide has demonstrated cardioprotective effects, but the underlying molecular mechanisms require further elucidation.

Purpose of the Study:

  • To investigate the role of HSP90-mediated inhibition of complement C5a/nuclear factor-kappa B (NF-κB) signaling in liraglutide-induced cardioprotection.
  • To determine if targeting this pathway can enhance the protective effects of liraglutide.

Main Methods:

  • Rat hearts subjected to 30 minutes of ischemia and 2 hours of reperfusion.
  • Groups included ischemia/reperfusion (I/R), sham, liraglutide preconditioning (LP), LP with HSP90 inhibitor (geldanamycin), and LP with C5a receptor antagonist (PMX53).
  • Assessed cardiac injury, C5a/NF-κB activation, and inflammatory markers.

Main Results:

  • Liraglutide preconditioning significantly reduced cardiomyocyte apoptosis, infarct size, and cardiac enzyme release.
  • These protective effects correlated with decreased C5a levels, suppressed NF-κB signaling, and reduced inflammation, alongside increased HSP90 levels.
  • Inhibition of HSP90 abolished liraglutide's cardioprotection, while C5a antagonism enhanced it, confirming the pathway's involvement.

Conclusions:

  • HSP90 plays a critical role in liraglutide-mediated cardioprotection by inhibiting inflammatory responses and C5a/NF-κB signaling.
  • This mechanism attenuates ischemia/reperfusion-induced cardiomyocyte apoptosis by modulating pro-apoptotic (Bax) and anti-apoptotic (Bcl2) factors.
  • Targeting the HSP90/C5a/NF-κB pathway presents a promising therapeutic strategy for protecting the heart during ischemic events.