<p>Myocardial infarction (MI) is a leading cause of death. In this study, we appraised the protective mechanisms of cuminaldehyde, a natural monocyclic terpenoid, in isoproterenol-induced myocardial infarcted rats. Our study included four groups: Group 1: normal control, Group 2: cuminaldehyde (20&#xa0;mg/kg body weight) alone, Group 3: isoproterenol (100&#xa0;mg/kg body weight) induced MI, Group 4: MI + cuminaldehyde (20&#xa0;mg/kg body weight). Cardiac apoptosis and fibrosis were evaluated by biochemical analysis, transmission electron microscopy (TEM), ELISA, RT-PCR, and histopathology to explore the potential molecular mechanisms underlying MI protection by cuminaldehyde. Results of this study revealed that plasma thiobarbituric acid reactive substances (TBARS), heart rate, and serum cardiac troponins-T and -I were raised; heart superoxide dismutase and catalase were reduced in isoproterenol-induced MI rats. Moreover, heart lysosomal TBARS and serum and heart lysosomal enzymes were enhanced. TEM study revealed a damaged heart lysosome. By RT-PCR, the expression of B-cell lymphoma-2 (Bcl-2), B-cell lymphoma-extra large (Bcl-xL), B-cell lymphoma-2 x (Bax), cytochrome <i>c</i> (Cyt<i>.c</i>), caspase-9, caspase-3, matrix metalloproteinase-2 (MMP-2), and matrix metalloproteinase-9 (MMP-9) was altered in the myocardium of MI rats. ELISA results revealed elevated serum MMP-2 and MMP-9. Further, histopathology of the heart revealed an accumulation of collagen. Nevertheless, MI rats treated with cuminaldehyde orally, daily for 21&#xa0;days, reduced oxidative stress, thereby inhibiting apoptosis and fibrosis. Moreover, RT-PCR analysis of Bax/Bcl-2/Bcl-xL/Cyt.<i>c</i>/caspase-9/caspase-3, and MMP-2/MMP-9 pathways demonstrated the molecular mechanisms responsible for the anti-apoptotic and anti-fibrotic potential of cuminaldehyde and mitigated the MI provoked by isoproterenol.Therefore, cuminaldehyde may be a promising phytopharmacological agent for MI therapy.</p>