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Related Experiment Video

Updated: Mar 10, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
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Complement and sepsis-induced heart dysfunction.

Fatemeh Fattahi1, Peter A Ward1

  • 1Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, United States.

Molecular Immunology
|December 10, 2016
PubMed
Summary
This summary is machine-generated.

Sepsis causes reversible heart dysfunction by activating C5a and its receptors on heart cells. Blocking C5a protects heart function during sepsis, suggesting new therapeutic strategies.

Keywords:
C5aR1C5aR2 (GPR77)Complement C5aNa(+)/Ca(2+) exchanger (NCX)Na(+)/K(+)-ATPaseSarco/endoplasmic reticulum Ca(2+)-ATPase 2 (SERCA2)

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Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Sepsis frequently leads to cardiac dysfunction in humans and animal models.
  • This sepsis-induced cardiac dysfunction is typically reversible upon recovery.
  • The complement system component C5a and its receptors are implicated in sepsis pathophysiology.

Purpose of the Study:

  • To investigate the role of C5a and its receptors (C5aR1, C5aR2) in sepsis-induced cardiac dysfunction.
  • To explore the molecular mechanisms underlying C5a-mediated cardiac impairment.
  • To evaluate the therapeutic potential of targeting the C5a pathway for cardiac protection during sepsis.

Main Methods:

  • In vivo and in vitro experimental models of sepsis.
  • Administration of a neutralizing antibody against C5a.
  • Assessment of cardiomyocyte (CM) function, contractility, and relaxation.
  • Measurement of key proteins involved in CM homeostasis, including Na+/K+-ATPase, SERCA2, and NCX.

Main Results:

  • C5a generation and its interaction with C5a receptors on CMs are critical for sepsis-induced cardiac dysfunction.
  • C5a signaling impairs CM contractility, relaxation, and Na+/K+-ATPase activity.
  • C5aR blockade significantly attenuates cardiac dysfunction and preserves CM homeostatic proteins (SERCA2, NCX) during sepsis.

Conclusions:

  • The C5a-C5a receptor axis plays a pivotal role in mediating cardiac dysfunction during sepsis.
  • Targeting C5a offers a promising therapeutic strategy to protect the heart from sepsis-induced damage.
  • Understanding these molecular interactions provides insights for developing novel treatments for sepsis complications.