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NADPH oxidase contributes to conversion of cardiac myocytes to a proinflammatory phenotype in sepsis

Jun Wu1, Hu Xu, Min Yang

  • 1Lawson Health Research Institute, Department of Medical Biophysics, University of Western Ontario, Canada.

Free Radical Biology & Medicine
|March 3, 2009
PubMed

Insights

NADPH oxidase activation in sepsis drives cardiomyocyte inflammation and polymorphonuclear leukocyte (PMN) infiltration. Blocking this enzyme prevents these sepsis-induced cardiac changes, highlighting its therapeutic potential.

Area of Science:

  • Cardiovascular Biology
  • Inflammation Research
  • Molecular Medicine

Background:

  • Sepsis-induced myocardial dysfunction involves polymorphonuclear leukocyte (PMN) infiltration.
  • The role of NADPH oxidase in cardiomyocyte reprogramming during sepsis is not fully understood.

Purpose of the Study:

  • To investigate the role of NADPH oxidase in sepsis-induced cardiomyocyte proinflammatory phenotype.
  • To assess NADPH oxidase's involvement in cardiomyocyte CXC chemokine production and PMN migration.

Main Methods:

  • In vitro study using cardiac myocytes treated with septic plasma.
  • Evaluation of NADPH oxidase activity (p47phox phosphorylation, O(2)(-) production).
  • Assessment of NF-kappaB and p38 MAP kinase pathways using blockade strategies.

Main Results:

  • Septic plasma activated NADPH oxidase and induced a proinflammatory cardiomyocyte phenotype, both prevented by NADPH oxidase blockade.
  • NF-kappaB nuclear translocation increased with septic plasma, inhibited by NADPH oxidase blockade.
  • NADPH oxidase blockade prevented IKK phosphorylation but not p65 phosphorylation; p38 MAP kinase was not involved in the NADPH oxidase pathway.

Conclusions:

  • NADPH oxidase activation is critical for sepsis-induced cardiomyocyte proinflammatory phenotype.
  • Two distinct pathways mediate cardiomyocyte reprogramming in sepsis: NADPH oxidase-IKK and p38 MAP kinase-p65.
  • Targeting NADPH oxidase may offer a strategy to mitigate sepsis-induced cardiac dysfunction.

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