Research Paper Volume 13, Issue 5 pp 6625—6633
Liraglutide preconditioning attenuates myocardial ischemia/ reperfusion injury via homer1 activation
- 1 Reproductive Medicine Center, Shanxi Maternal and Child Health Care Hospital, Affiliated of Shanxi Medical University, Taiyuan 030001, China
- 2 Clinical Laboratory, Shanxi Provincial People’s Hospital, Affiliated of Shanxi Medical University, Taiyuan 030001, China
Received: July 17, 2020 Accepted: November 11, 2020 Published: February 1, 2021https://doi.org/10.18632/aging.202429
How to Cite
Copyright: © 2021 Cui et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Myocardial infarction (MI) is one of most common cardiovascular diseases, and ischemia/reperfusion (I/R) injury is one of the risk factors for severe myocardial injury and dysfunction, even leading to high mortality of myocardial infarction. Liraglutide, a novel glucagon-like peptide 1 (GLP-1) analogue, has been reported to reduce cardiac rupture and infarct size and improve cardiac function in normal and diabetic rodents, however, the mechanisms of liraglutide on cardiomyocytes is not clear. The current research was designed to investigate the hypothesis that liraglutide would protect cardiomyocytes through regulating homer1 expression under hypoxia/reoxygenation (H/R) condition. The results of the present study indicated liraglutide reduced hypoxia-reoxygenation induced cell death and attenuated intracellular calcium overload in H9C2 cardiomyocytes under H/R condition. Moreover, liraglutide significantly increased the Homer1 protein expression, and this protection might be related to Homer1-dependent regulation of endoplasmic reticulum (ER) calcium homeostasis. Taken together, liraglutide protects H9C2 cell against H/R induced cell injury, and this protective effect may inhibit intracellular calcium overload to some extent, through Homer1-dependent regulation of ER calcium homeostasis.