THE IMPACT OF LEPTIN ON VENTRICULAR MYOCYTE APOPTOSIS AND REMODELING IN ATHLETES: INVESTIGATING THE MIR-27A/B-3P/MFF/GTPASE OPA1 AXIS

Abstract

Background: Overexpressed leptin produces deleterious ventricular remodeling and cardiomyocyte apoptosis, but its regulatory mechanism is unclear. Objective: To investigate the mechanism of miR-27a/b-3p targeting MFF/GTPase OPA1 to regulate leptin expression and affect ventricular myocyte apoptosis and ventricular remodeling. Methods: 63 athletic patients with myocardial infarction and 65 normal controls were recruited in our hospital. Leptin, miR-27a-3p, miR-27b-3p, MFF, and GTPase OPA1 were then detected in serum using RT-PCR, along with the expression of apoptotic factors Bcl-2, Bax, Caspease3, and P53. There were measurements of the echocardiographic parameters of ventricular remodeling. Ejection fraction (EF), end-diastolic diameter (LVEDD), left ventricular ejection time, and short-axis shortening rate (LVFS) were all measured. BNP, NT-proBNP, AngII, cTnI, and MYO myocardial index values are also included. Finally, the survival curve of the athletic patients during the follow-up period was drawn. Results: A significant rise in leptin expression was seen in athletic patients with myocardial infarction when compared to that found in healthy controls, as was an increase in miR-27a-3p and miR-27b-3p expression, as well as elevated levels of MFF and the GTPase OPA1. Athletic patients with myocardial infarction had lower levels of the anti-apoptotic factor Bcl-2, whereas the pro-apoptotic factors Bax, Caspease3, and P53 had higher levels. In addition, LVEF and LVFS parameters of ventricular remodeling were decreased, LVEDD and LAD parameters were increased, and the levels of myocardial function indexes ANP, BNP, NT-proBNP, AngⅡ, cTnI and MYO were significantly increased (P<0.01). The survival rate of athletic patients with myocardial infarction was significantly decreased during follow-up (P<0.01). Conclusion: The miR-27a/b-3p/MFF/GTPase OPA1 axis can induce ventricular myocyte apoptosis and ventricular remodeling in athletic patients with myocardial infarction by promoting the expression of leptin, indicating that leptin can be used as a key marker of myocardial infarction. Personalized treatment.