Coenzyme Q10 Modulates Gene Expression in Myocardial Infarction Induced by Isoproterenol

Cardiac remodeling involves alterations in gene expression, molecular, cellular, and interstitial changes that ultimately affect heart function. Coenzyme Q10 (CoQ10) plays a critical role in the mitochondrial electron transport chain, which is essential for ATP production. This study aimed to evaluate the effect of CoQ10 on myocardial infarction (MI) in male rats induced by isoproterenol (ISO). The rats were divided into four groups: control, CoQ10-treated, ISO-treated, and CoQ10+ISO-treated. Various biochemical markers were evaluated, including liver function indicators (AST, ALT, ALP, albumin, and total protein), cardiac biomarkers, electrolytes, TNF levels, oxidative stress (malondialdehyde [MDA]), and antioxidant markers (superoxide dismutase [SOD], reduced glutathione [GSH]). In addition, qPCR was used to measure the expression of key genes involved in angiogenesis (vascular endothelial growth factor [VEGF]), migration (matrix metalloprotease 9 [MMP9]), and antioxidants (heme oxygenase-1 [HO-1]) in heart tissue. CoQ10 treatment in ISO-treated rats resulted in a significant reduction in liver injury, as evidenced by improved liver function markers, decreased MDA levels, elevated GSH and SOD levels, and upregulated VEGF, MMP9, and HO-1 expression. These findings suggest that CoQ10 has a protective role against myocardial injury caused by the ISO-induced model.