Why the study?
Paroxetine is known to inhibit GRK2, which is linked to cardiovascular disease progression, but its protective effect on post-MI remodeling has not been elucidated.
Does paroxetine prevent post-MI ventricular remodeling in an animal model of myocardial infarction?
Does paroxetine prevent post-MI ventricular remodeling in an animal model of myocardial infarction?
In an animal model of myocardial infarction, paroxetine attenuated cardiac injury and post-MI remodeling, suggesting a potential cardioprotective role via GRK2 inhibition.
Paroxetine attenuated post-MI remodeling in rodents; leaves open whether GRK2 inhibition benefits patients.
BACKGROUND: Post-myocardial infarction (MI) remodeling involves various structural and functional changes, such as inflammation and fibrosis. Upregulation of G protein-coupled receptor kinase 2 (GRK2) is linked to the progression of cardiovascular diseases, including myocardial infarction. The inhibitory effects of paroxetine on GRK2 are recognized, yet its protective effect on post-MI remodeling has not been elucidated. Here, we investigated the cardioprotective effect of paroxetine in an animal model of MI, focusing on post-MI cardiac remodeling and comparing its effect to a β-blocker and an angiotensin receptor antagonist. METHODS: ) on days 16 and 17. Cardioprotective effects were determined by assessing markers of cardiac injury, histopathology, inflammation, oxidative stress, and fibrosis. Statistical analysis performed using a one-way analysis of variance, followed by an appropriate post hoc test, the differences between the groups were considered significant when the (P < 0.05). RESULTS: Paroxetine significantly attenuated cardiac injury biomarkers including serum Tn-I and CK-MB levels. In terms of cardiac remodeling, paroxetine significantly reduced the relative HW/BW index and the plasms FGF23 level. Furthermore, it modulated markers of fibrosis, inflammation, and oxidative stress. CONCLUSION: The current findings suggest that pre-treatment with paroxetine may exert a beneficial effect that protects against post-MI remodeling, including modulating fibrotic, inflammatory, and angiogenesis-related factors. Therefore, the current findings show the promising role of paroxetine as a cardioprotective that attenuates post-MI remodeling processes.
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Alonazi et al. (2024) studied this question.
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