Unraveling the Mechanisms of Neutrophil Extracellular Trap Formation and the Role of Reactive Oxygen Species in Myocardial Bridging.

Authors

Admin Šenderović, Semira Galijašević

Published in

Anatolian journal of cardiology. Sep 24, 2026. Epub Sep 24, 2026.

Abstract

Myocardial bridging (MB) is a congenital coronary anomaly in which a segment of a coronary artery courses through the myocardium, resulting in systolic compression and alterations in coronary vasoreactivity. Consequently, morphological, functional, and hemodynamic changes may occur, with various clinical implications. Although traditionally considered a benign anatomical variant, accumulating evidence suggests an association between MB and endothelial dysfunction, oxidative stress, local inflammatory activation, and atherosclerotic plaque formation, predominantly in the arterial segment proximal to the bridge. Reduced wall shear stress in the proximal segment is associated with a pro-inflammatory and prooxidative vascular environment characterized by reduced nitric oxide (NO) bioavailability, despite increased endothelial nitric oxide synthase (eNOS) expression, consistent with impaired eNOS signaling and possible functional uncoupling, together with activation of reactive oxygen species-generating pathways. Myeloperoxidase (MPO), released from activated neutrophils, is a key mediator of oxidative vascular injury and may contribute to endothelial dysfunction by reducing NO bioavailability, generating highly reactive oxidants such as hypochlorous acid, and promoting oxidative endothelial injury. Hemodynamic alterations characteristic of MB may promote MPO activation and the MPO-H2O2 pathway, thereby facilitating mechanisms involved in neutrophil extracellular trap (NET) formation and contributing to the pro-inflammatory vascular environment. MPO- and NET-mediated pathways may represent biologically plausible contributors to endothelial dysfunction and proximal atherogenesis in MB. However, the role of these pathways in the pathophysiology of MB remains insufficiently investigated and should currently be regarded as a hypothesis rather than an established pathophysiological mechanism.

PMID:
42779493
Bibliographic data and abstract were imported from PubMed on 24 Sep 2026.

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