Is Ferroptosis and Oxidative Stress Involved in NSTEMI Patient’s?

Ali  Mirzaee; Maryam  Mehrpooya; Akram  Ranjbar; Sajad  Naghdi; Afsaneh  Familmotaghi; Seyed Saman  Talebi; Seyed Kianoosh  Hosseini

doi:10.18502/jthc.v21i1.21281

Ali Mirzaee Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran.
Maryam Mehrpooya Department of Clinical Pharmacy, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran.
Akram Ranjbar Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran.
Sajad Naghdi Farshchian Cardiovascular Subspecialty Medical Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Afsaneh Familmotaghi Farshchian Cardiovascular Subspecialty Medical Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Seyed Saman Talebi Department of Internal Medicine, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Seyed Kianoosh Hosseini Department of Cardiology, School of Medicine, Farshchian Cardiovascular Subspecialty Medical Center, Hamadan University of Medical Sciences, Hamadan, Iran.

DOI: https://doi.org/10.18502/jthc.v21i1.21281

Keywords: Non–ST-Segment Elevation Myocardial Infarction; Oxidative Stress; Ferroptosis

Abstract

Background: Ischemic heart disease is the leading cause of death worldwide. Oxidative stress plays a key role in myocardial infarction (MI). Ferroptosis, a type of iron-dependent regulated cell death caused by lipid peroxide accumulation, has been identified as a key mechanism in ischemic injury. This study aimed to investigate the association between oxidative stress and ferroptosis in patients with non–ST-segment-elevation myocardial infarction (NSTEMI).

Methods: In this case-control study, 25 patients with NSTEMI and 25 controls were included. In serum samples, cardiac markers (troponin I and CK-MB), oxidative stress biomarkers including lipid peroxidation (LPO), total antioxidant capacity (TAC), total thiol groups (TTG), superoxide dismutase (SOD) activity, glutathione peroxidase (GPx) activity, and iron and ferritin levels were measured.

Results: In patients with NSTEMI, serum levels of cardiac markers (troponin I and CK-MB), LPO, iron, and ferritin were significantly higher than in controls. In contrast, TAC, TTG, and SOD and GPx activities were significantly lower in patients with NSTEMI.

Conclusion: This study demonstrated a possible role of oxidative stress in the pathophysiology of NSTEMI. Elevated iron and LPO levels and reduced GPx activity may contribute to cardiac cell death through ferroptosis.