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Review
. 2022 Dec 8;11(24):3964.
doi: 10.3390/cells11243964.

Protective Biomolecular Mechanisms of Glutathione Sodium Salt in Ischemia-Reperfusion Injury in Patients with Acute Coronary Syndrome-ST-Elevation Myocardial Infarction

Affiliations
Review

Protective Biomolecular Mechanisms of Glutathione Sodium Salt in Ischemia-Reperfusion Injury in Patients with Acute Coronary Syndrome-ST-Elevation Myocardial Infarction

Alessio Arrivi et al. Cells. .

Abstract

Ischemia-Reperfusion Injury (IRI) is responsible for adverse outcomes in patients with ST-Elevation Myocardial Infarction (STEMI). Oxidative stress, resulting from the production of Reactive Oxygen Species (ROS) and low availability of Glutathione (GSH), are the two main mediators of IRI. The effectiveness of exogenous antioxidant therapy in this scenario is still debated, since the encouraging results obtained in animal models have not been fully reproduced in clinical studies. In this review we focus on the role of GSH, specifically on the biomolecular mechanisms that preserve myocardial cells from damage due to reperfusion. In this regard, we provide an extensive discussion about GSH intrinsic antioxidant properties, its current applications in clinical practice, and the future perspectives.

Keywords: STEMI; angioplasty; glutathione; primary PCI; reperfusion injury.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The pathophysiology of IRI. Abbreviations. STEMI: ST-elevation myocardial infarction, pPCI: primary PCI, NO: nitric oxide, ROS: Reactive Oxygen Species, and GSH: glutathione.
Figure 2
Figure 2
Glutathione Redox cycle. Abbreviations. GSSG: Oxidized Glutathione, GSH: Reduced Glutathione.

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