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Related Experiment Video

Updated: Jan 16, 2026

Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension
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GP130 Antagonism Enhances Porcine RV Function.

Jenna B Mendelson1, Jacob D Sternbach2, Minwoo Kim2

  • 1Department of Integrative Biology and Physiology (J.B.M.), University of Minnesota, Minneapolis, MN.

Circulation Research
|October 1, 2025
PubMed
Summary

The small molecule SC144 improves right ventricular (RV) function in a large animal model by reducing inflammation and metabolic dysfunction. This study shows SC144 enhances RV ejection fraction and preserves cardiomyocyte health.

Keywords:
autophagyinflammationlipidomicsmetabolismventricular function, right

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Area of Science:

  • Cardiovascular Research
  • Translational Medicine
  • Pharmacology

Background:

  • Right ventricular (RV) dysfunction is a significant risk factor for mortality in cardiovascular diseases, yet effective therapies remain limited.
  • The small molecule SC144 has shown promise in improving RV function in rodent models through anti-inflammatory and metabolic pathways.
  • The efficacy and underlying molecular mechanisms of SC144 in a large animal model of RV dysfunction require investigation.

Purpose of the Study:

  • To evaluate the therapeutic potential of SC144 in a translational large animal model of RV dysfunction.
  • To elucidate the molecular and cellular mechanisms by which SC144 improves RV function.
  • To assess the impact of SC144 on RV hemodynamics, cellular composition, metabolism, and mitochondrial function.

Main Methods:

  • Pulmonary artery banding (PAB) was performed in pigs to induce RV dysfunction.
  • PAB pigs were randomized to receive daily SC144 injections or vehicle control for 3 weeks.
  • Comprehensive analyses included cardiac MRI, right heart catheterization, single-nucleus RNA sequencing, electron microscopy, phosphoproteomics, lipidomics, metabolomics, and quantitative proteomics.

Main Results:

  • SC144 significantly improved RV ejection fraction without altering RV afterload.
  • SC144 treatment blunted PAB-induced increases in RV macrophage, lymphocyte, and pericyte/endothelial cell abundances and reduced macrophage infiltration.
  • SC144 counteracted PAB-induced downregulation of cardiomyocyte metabolic genes, normalized mTORC1 signaling, improved mitochondrial morphology, restored fatty acid metabolism, and rebalanced pericyte-endothelial cell interactions.

Conclusions:

  • GP130 antagonism with SC144 mitigates RV dysfunction by reducing inflammation, preserving cardiomyocyte metabolism, and restoring cellular homeostasis.
  • SC144 demonstrates significant therapeutic potential for RV dysfunction in a large animal model, offering a promising avenue for clinical translation.
  • The study highlights SC144's multifaceted effects on RV pathophysiology, including anti-inflammatory, metabolic, and vascular protective mechanisms.