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Drp1/Fis1 interaction mediates mitochondrial dysfunction in septic cardiomyopathy.

Bereketeab Haileselassie1, Riddhita Mukherjee1, Amit U Joshi2

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Sepsis causes heart dysfunction by damaging mitochondria. Inhibiting the Drp1/Fis1 interaction protected heart cells and improved function in mice, reducing mortality from septic cardiomyopathy.

Keywords:
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Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Sepsis Research

Background:

  • Mitochondrial dysfunction is central to septic cardiomyopathy.
  • Dynamin-related protein 1 (Drp1) and fission 1 (Fis1) are implicated in neurodegenerative mitochondrial failure.
  • The role of Drp1/Fis1 in sepsis-induced cardiomyopathy is largely unknown.

Purpose of the Study:

  • To investigate the role of Drp1/Fis1 interaction in sepsis-mediated mitochondrial dysfunction and cardiac failure.
  • To test if inhibiting Drp1/Fis1 interaction can mitigate sepsis-induced cardiac damage.

Main Methods:

  • Lipopolysaccharide (LPS) was used to induce septic cardiomyopathy in H9C2 cardiomyocytes and Balb/c mice.
  • Mitochondrial function (membrane potential, respiration, oxidative stress) and morphology were assessed.
  • Cardiac function was measured using echocardiography.
  • The effect of P110, an inhibitor of Drp1/Fis1 interaction, was evaluated.

Main Results:

  • LPS treatment decreased mitochondrial respiration and membrane potential, increasing oxidative stress in cardiomyocytes.
  • Inhibition of Drp1/Fis1 with P110 attenuated oxidative stress and preserved membrane potential.
  • LPS-induced cardiac dysfunction in mice correlated with mitochondrial fragmentation.
  • P110 treatment reduced mitochondrial fragmentation, improved cardiac function, and decreased mortality.

Conclusions:

  • Sepsis impairs cardiac mitochondrial function, increasing oxidative stress and causing pathologic fission.
  • Inhibiting the Drp1/Fis1 interaction with P110 demonstrated protective effects in vitro and in vivo.
  • The Drp1/Fis1 interaction is a critical mediator of septic cardiomyopathy and a potential therapeutic target.