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

Ferroptosis (iron-dependent lipid peroxidation-driven cell death) is implicated in ischemic injury.NSTEMI patients showed significantly higher oxidative stress (↑LPO) and iron overload (↑iron, ↑ferritin) vs controls.Antioxidant defenses were reduced in NSTEMI (↓TAC, ↓TTG, ↓SOD, ↓GPx activity).This biomarker pattern supports ferroptosis activation contributing to myocardial injury in NSTEMI.

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).

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.

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.

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.