Key result
Chronic sleep disruption worsens post-MI myocardial injury and reduces cardioprotective TIMP-1 levels.
Why the study?
Epidemiological studies link sleep duration to cardiovascular diseases including CAD, motivating investigation into how sleep disruption prior to MI affects cardiac injury and the mediating role of matrix metalloproteinases.
Does chronic sleep disruption for 14 days prior to isoproterenol-induced myocardial infarction worsen cardiac injury and alter MMP-2 activity and TIMP-1 levels in adult male Wistar rats?
Does chronic sleep disruption for 14 days prior to isoproterenol-induced myocardial infarction worsen cardiac injury and alter MMP-2 activity and TIMP-1 levels in adult male Wistar rats?
Chronic sleep disruption prior to isoproterenol-induced myocardial infarction in rats exacerbates myocardial fiber disorganization and reduces the TIMP-1/β-actin ratio, suggesting an MMP/TIMP imbalance as a potential mechanism linking sleep disruption to worsened cardiac injury.
Sleep disruption may worsen experimental MI injury via MMP/TIMP imbalance; leaves open human relevance and clinical translation.
Epidemiological studies have demonstrated an association between sleep duration and various health risk factors, including obesity and cardiovascular diseases, particularly coronary artery disease (CAD). The present study aimed to examine the impact of sleep disruption (SD) prior to myocardial infarction (MI) on cardiac injury, with a specific focus on matrix metalloproteinases (MMPs) as potential mediators of this relationship. Using a controlled animal model, adult male Wistar rats were subjected to chronic SD for 14 days, followed by induction of MI via isoproterenol administration. The activities of MMP-2 and the level of tissue inhibitor of metalloproteinase-1 (TIMP-1) were assessed, alongside histological evaluations of cardiac tissue and oxidative stress markers. Results indicated a significant reduction in the TIMP-1/β-actin ratio in the MI and SD+MI groups, with a more pronounced decrease in the SD+MI group, and an increase in MMP-2 activity in the MI group compared to the control group, suggesting an imbalance between MMPs and TIMPs that may contribute to myocardial damage. Histological analysis revealed notable disorganization of myocardial fibers, which appeared more severe in the SD+MI group, highlighting the detrimental impact of SD on cardiac tissue integrity. Although no significant alterations in oxidative stress markers were detected, the findings underscore the detrimental role of SD in cardiovascular health and suggest that this imbalance between MMPs and TIMPs could serve as a potential mechanism involved in cardiovascular diseases associated with SD.
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Parsazadegan et al. (2026) studied Isoproterenol-induced myocardial infarction (animal model). Chronic sleep disruption prior to isoproterenol-induced myocardial infarction vs. Control group and myocardial infarction without sleep disruption was evaluated on MMP-2 activity, TIMP-1/β-actin ratio, cardiac tissue histology, and oxidative stress markers. Chronic 14-day sleep disruption prior to isoproterenol-induced MI in rats significantly reduced the TIMP-1/β-actin ratio and worsened myocardial fiber disorganization compared to MI alone.
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