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Related Experiment Videos

Enhanced Glycolytic Metabolism Contributes to Cardiac Dysfunction in Polymicrobial Sepsis.

Zhibo Zheng1,2, He Ma1,3, Xia Zhang1

  • 1Departments of Surgery.

The Journal of Infectious Diseases
|April 4, 2017
PubMed
Summary

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Inhibiting hexokinase with 2-deoxy-d-glucose (2-DG) improved cardiac function and survival in a mouse model of sepsis. This intervention reduced inflammation and apoptosis, highlighting glycolysis

Area of Science:

  • Biochemistry
  • Immunology
  • Cardiology

Background:

  • Sepsis affects over 40% of patients, leading to cardiac dysfunction and high mortality.
  • Glycolytic metabolism is crucial for immune cell defense and inflammation.
  • Toll-like receptor activation enhances immune cell glycolysis.

Purpose of the Study:

  • To investigate the therapeutic potential of inhibiting hexokinase, a key glycolytic enzyme, in septic cardiomyopathy.
  • To determine if 2-deoxy-d-glucose (2-DG) can mitigate sepsis-induced cardiac dysfunction.

Main Methods:

  • Male C57B6/J mice underwent cecal ligation and puncture (CLP) to induce sepsis.
  • Mice were treated with varying doses of 2-DG before CLP.
  • Cardiac function was assessed via echocardiography; serum cytokines, lactate, and myocardial gene expression were analyzed.
Keywords:
2-deoxy-D-glucosecardiomyopathyglycolysisinflammatory responses.sepsis

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Main Results:

  • 2-DG treatment significantly attenuated sepsis-induced cardiac dysfunction, improving ejection fraction and fractional shortening.
  • 2-DG administration enhanced survival, reduced organ injury, and lowered inflammatory markers (TNF-α, IL-1β) and lactate.
  • Myocardial expression of Sirt1/Sirt3 was enhanced, while apoptotic markers (Bak, Bax) and JNK phosphorylation were suppressed.

Conclusions:

  • Glycolytic metabolism is a key mediator of septic cardiomyopathy.
  • Inhibiting hexokinase with 2-DG offers a potential therapeutic strategy for sepsis.
  • Mechanisms involve regulating inflammatory and apoptotic signaling pathways.