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Related Experiment Video

Updated: Nov 24, 2025

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
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Different DOACs Control Inflammation in Cardiac Ischemia-Reperfusion Differently.

Ihsan Gadi1, Sameen Fatima1, Ahmed Elwakiel1

  • 1Institute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostics, University Hospital, Leipzig, Germany (I.G., S.F., A.E., S.N., M.M.A.-D., R.R., J.M., D.G., R.B., S.K., B.I., K.S.).

Circulation Research
|December 23, 2020
PubMed
Summary

Direct oral anticoagulants targeting factor Xa (fXa) or factor IIa (fIIa) show differential impacts on gene expression and inflammation during myocardial injury. Factor Xa inhibition uniquely reduces sterile inflammation and fibrosis, independent of anticoagulant effects.

Keywords:
inflammasomesinflammationmyocardial infarctionthrombinthrombosis

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Area of Science:

  • Cardiovascular Research
  • Coagulation Cascade Biology
  • Inflammation and Immunity

Background:

  • Thrombin (fIIa) is central to thrombus formation.
  • Other proteases like factor Xa (fXa) and activated protein C (aPC) modulate intracellular signaling via distinct receptors.
  • Understanding differential protease inhibition effects is crucial for treating cardiovascular diseases.

Purpose of the Study:

  • To investigate the distinct effects of fXa versus fIIa inhibition on gene expression and inflammation in myocardial ischemia-reperfusion injury.
  • To elucidate the mechanisms underlying these differential responses.

Main Methods:

  • Mice with myocardial ischemia-reperfusion injury were treated with direct fXa inhibitors (fXai) or direct fIIa inhibitors (fIIai).
  • Comparable anticoagulant effects were confirmed via ex vivo and in vivo assays.
  • Gene expression was analyzed using RNA sequencing; infarct size, aPC generation, and inflammatory markers were quantified.

Main Results:

  • Both fXai and fIIai reduced infarct size comparably.
  • fXai, but not fIIai, significantly inhibited sterile inflammation by reducing pro-inflammatory cytokines (IL-1β, IL-6, TNFα) and NF-κB/inflammasome activation.
  • fXai treatment led to reduced myocardial fibrosis and increased in vivo aPC generation compared to fIIai.

Conclusions:

  • Specific inhibition of coagulation proteases yields distinct cellular responses beyond their anticoagulant properties.
  • Factor Xa inhibition offers a unique anti-inflammatory benefit in myocardial ischemia-reperfusion injury, mediated partly through activated protein C signaling.
  • Targeting specific coagulation proteases may provide tailored therapeutic strategies for cardiovascular conditions.