Journal Article Epublish 2 citations
PubMed: 39595040 DOI: 10.3390/biomedicines12112474
Early Cardiac Ischemia-Reperfusion Injury: Interactions of Autophagy with Galectin-3 and Oxidative Stress.
Biomedicines 12(11)
Authors: Suhail Al-Salam, Satwat Hashmi, Govindan S Jagadeesh, Manjusha Sudhadevi, Aktham Awwad, Abderrahim Nemmar
Affiliations
- Department of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 15551, United Arab Emirates.
- Department of Biological and Biomedical Sciences, Agha Khan University, Karachi City 74000, Pakistan.
- Department of Laboratory Medicine, Tawam Hospital, Al Ain P.O. Box 5674, United Arab Emirates.
- Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 15551, United Arab Emirates.
Abstract
: Cardiovascular diseases are the leading cause of death worldwide, including the United Arab Emirates. Ischemia-reperfusion (IR) injury results in the death of cardiac myocytes that were viable immediately before myocardial reperfusion. We aim to investigate the role of galectin-3 (Gal-3) in autophagy during ischemia-reperfusion injuries. : Male C57B6/J and Gal-3 knockout (KO) mice were used for the murine model of IR injury. Heart samples and serum were collected 24 h post-IR and were processed for immunohistochemical and immunofluorescent labeling and an enzyme-linked immunosorbent assay. : There was a significant increase in left ventricle (LV) concentrations of Gal-3 in Gal-3 wild-type mice compared to sham mice. There were significantly higher concentrations of LV autophagy proteins and phospho-AMPK in IR Gal-3 KO mice than in IR Gal-3 wild-type mice, compared to lower concentrations of LV phospho-mTOR and p62 in IR Gal-3 KO than in IR wild-type mice. Antioxidant activities were higher in the LVs of IR Gal-3 wild-type mice, while oxidative stress was higher in the LVs of IR Gal-3 KO mice. : Our study supports the interaction of Gal-3 with autophagy proteins, oxidative stress, and antioxidant proteins and demonstrates that the absence of Gal-3 can enhance autophagy in the heart after IR injury.
MeSH
Autophagy, Galectins, Heart, Stress, Physiological, Galectin 3, Oxidative Stress, Reperfusion, Reperfusion Injury, Ischemia