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FAQ: Neutrophil Extracellular Traps in Ischemia-Reperfusion Injury
This FAQ explains how neutrophils and their web-like structures (NETs) drive the paradoxical damage that occurs when blood flow is restored after ischemia, and explores their potential as biomarkers and therapeutic targets in heart attack, stroke, and organ transplantation.
IRI is the tissue damage that occurs when blood flow is restored after a period of ischemia (restricted blood supply). While reperfusion is essential for survival, it can trigger inflammation, oxidative stress, and microvascular dysfunction, often worsening the injury.
NETs are web-like structures composed of DNA, histones, and enzymes released by activated neutrophils. In sterile IRI, excessive NET formation can damage endothelial cells, promote microthrombi, and amplify inflammation, thereby intensifying tissue injury.
NET-mediated IRI affects multiple organs, including the heart, brain, kidney, liver, and lungs. It also plays a role in graft dysfunction after transplantation.
In the brain, NETs can obstruct cerebral microvessels and disrupt the blood-brain barrier, contributing to poor neurological recovery even when the main vessel is reopened.
The NET-organ axis refers to the phenomenon where NET-driven inflammation and thrombosis extend damage beyond the original injury site, potentially leading to multiple organ dysfunction syndrome (MODS).
Potential biomarkers include cell-free DNA (cfDNA), citrullinated histone H3 (CitH3), and myeloperoxidase-DNA (MPO-DNA) complexes. These may help assess disease severity and response to therapy.
No, NETs are not uniformly harmful. Their effects depend on the organ, disease stage, and local microenvironment. In some contexts, they may help trap microbes, but in sterile injury, excessive NET formation is damaging.
The review was published in Burns & Trauma on 15 June 2026 by researchers from Chongqing University Central Hospital, Chongqing University, University Hospital Essen, University of Duisburg-Essen, and Ludwig-Maximilians-University Munich.
The review suggests that targeting NET formation or promoting NET degradation could be a therapeutic strategy to protect organs during reperfusion. Identifying appropriate timing and organ-specific mechanisms is critical for success.