Influence of Sleep Disruption Before Myocardial Infarction on Cardiac Injury Following Isoproterenol Administration: Insights into Matrix Metalloproteinases

Authors

  • Tannaz Parsazadegan Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Kamran Rakhshan Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Mahdieh Faghihi Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Fataneh Esmaeili Department of Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Shadi Sadat Seyyed Ebrahimi Department of Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Alireza Imani Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

DOI:

https://doi.org/10.18502/acta.v64i9.22946

Keywords:

Sleep disruption; Myocardial infarction; Matrix metalloproteinases

Abstract

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.

Published

2026-10-14

Issue

Section

Articles