The study looked at a tiny mitochondrial peptide called MOTS‑c in heart‑attack patients. Overall levels of MOTS‑c weren’t different from healthy people, but the peptide changed over time after a heart attack and was linked to higher platelet counts and troponin I, two markers of heart damage. This hints that MOTS‑c might help doctors track heart‑attack severity, but it doesn’t tell us how to use it for self‑treatment.

Myocardial infarction (MI) is a disease characterised by myocardial necrosis due to acute and prolonged ischaemic hypoxia in the coronary arteries. MOTS-c is a mitochondrial- derived peptide that has been reported to have protective effects on cardiac tissue. Although this peptide is thought to be decreased in various diseases and can serve as a potential biomarker, current studies remain limited. This study aimed to evaluate how the post-treatment process affects circulating MOTS- c peptide levels in myocardial infarction patients. For this purpose, patients without obstructive coronary lesions on angiography were included in the control group, while those with significant obstructive coronary lesions on angiography were included in the infarction group. Routine biochemistry tests were performed using an autoanalyzer. Besides, serum MOTS-c levels were measured using ELISA. Our findings showed CRP, ESR, and troponin I levels to be higher in the MI group compared to the control group. Also, there was no significant change in MOTS-c levels between the control and the MI group, while time-dependent changes (day 0, day 3, and day 30) occurred within the MI group. However, a negative correlation was found between MOTS-c and platelet levels in the MI group at day 0 (r: -0.4417, p =0.0450). Similarly, MOTS-c was found to be negatively correlated with troponin I in the MI group at day 3 (r: -0.4571, p =0.0372). The negative correlation of MOTS-c level with both platelet and troponin I has shown that this peptide may contribute to the diagnostic and therapeutic evaluation of the MI process along with other parameters.