The investigation of the role in the heart ischemia and reperfusion injury of a new hormone known as meteorin-like

Myocardial infarction (MI) is a heart disease with a high mortality and morbidity rate. Although it is known that exercise has protective effects on MI, the mediating molecules acting in this process are not known precisely. In our study, it is aimed to investigate the role of METRNL, which is known to be synthesized in heart and muscle tissue, in cardiac ischemic injury. METRNL levels in human control (n=200) and MI serum samples (n = 200) were assessed using ELISA assay. Wistar albino rats were divided into six groups as control, I\R, exercise (E), I\R + E, I\R + M and I\R+ E+M as six animals in each group. A 6-week treadmill running exercise was performed for the exercise groups. Expression levels of METRNL and MB related genes in heart and muscle tissues were evaluated by qRT-PCR. METRNL, IL-4, CK-MB and ATP ELISA levels in heart, muscle and serum samples were performed using ELISA. The effect of METRNL on vascular contractions was determined by an isolated organ bath experiment. Human serum METRNL levels did not change in MI patients compared to the control. According to the control group, heart METRNL expression decreased significantly in the I/R group. Heart METRNL levels were normalized in all excercise groups. In the other groups according to the control, MB-related gene expressions in heart and muscle tissues were found to show significant changes. TFAM levels were significantly increased in the METRNL-treated groups. In the isolated organ bath experiment, METRNL significantly increased the vascular contractions at 12.5 μg / ml dose. In the present study, it was observed that the protective feature of exercise in I/R was associated with MB. It was found that METRNL decreased in I/R damage and that the exercise normalized this decrease. METRNL is thought to have protective properties by increasing TFAM levels, improving ECG findings and increasing vascular contractions in the rat cardiac I /R model.