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Cyclooxygenase-2 inhibition improves hypercholesterolemia-induced cardiac dysfunction.

Bernadett Kiss1, Regina N Nagy1, Gábor B Brenner1

  • 1Department of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvárad tér 4, Budapest H-1089, Hungary; Center for Pharmacology and Drug Research & Development, Semmelweis University, Nagyvárad tér 4, Budapest H-1089, Hungary.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|November 30, 2025
PubMed
Summary

Rofecoxib surprisingly improved hypercholesterolemia-induced heart dysfunction in rats. This study reveals rofecoxib

Keywords:
Cyclooxygenase-2 inhibitorHidden cardiotoxicityHypercholesterolemiaMyocardial reperfusion injuryPreclinical drug safety

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Area of Science:

  • Cardiovascular Pharmacology
  • Drug-Induced Cardiotoxicity
  • Metabolic Cardiomyopathy

Background:

  • Hidden cardiotoxicity manifests in diseased hearts.
  • Selective cyclooxygenase-2 inhibitors like rofecoxib can exhibit proarrhythmic hidden cardiotoxicity.
  • Metabolic comorbidities, such as hypercholesterolemia (HC), may worsen hidden cardiotoxicity.

Purpose of the Study:

  • To investigate the hidden cardiotoxic effects of rofecoxib in the context of hypercholesterolemia.
  • To determine if rofecoxib exacerbates or ameliorates cardiac dysfunction in hypercholesterolemic rats.
  • To explore the molecular mechanisms underlying rofecoxib's effects on the hypercholesterolemic heart.

Main Methods:

  • Rats were fed a high-cholesterol diet for 12 weeks to induce hypercholesterolemia.
  • Rats received rofecoxib treatment (5.12 mg/kg) for four weeks.
  • RNA sequencing was performed to analyze gene and miRNA expression changes in cardiac tissue.

Main Results:

  • Rofecoxib treatment surprisingly improved mild cardiac dysfunction induced by hypercholesterolemia.
  • Cardiac function markers, including end-diastolic pressure, stroke work, and mechanical efficiency, were restored by rofecoxib.
  • RNA sequencing revealed significant alterations in 28 miRNAs and 300 genes due to HC, with rofecoxib reversing changes in specific miRNAs (miR-27a-5p, miR-30d-5p) and genes (Cdc42ep4, Cox5, Cxcl9).

Conclusions:

  • This study provides the first evidence that rofecoxib can improve hypercholesterolemia-induced cardiac dysfunction.
  • The beneficial effects of rofecoxib involve modulation of gene expression profiles, including key regulators of its action.
  • Rofecoxib's impact on hidden cardiotoxicity in metabolic conditions warrants further investigation.