Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2026 Oct 20;17:1972426. doi: 10.3389/fimmu.2026.1972426

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2026 Chen and Zhu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Infographic illustrating a three-stage framework for NET-associated assessment and intervention in NEC: NET formation with neutrophil activation and biomarkers, NET persistence with impaired clearance, and downstream immunothrombotic tissue injury involving platelets, coagulation, and intestinal damage, each stage accompanied by potential intervention points and representative biomarkers. — NET-associated assessment and potential intervention framework in NEC. NET-associated processes in NEC are conceptually divided into three stages: NET formation, NET persistence or impaired clearance, and downstream immunothrombotic injury. Representative markers include tissue extracellular DNA with MPO/NE colocalization, H3cit, MPO–DNA/NE–DNA complexes, cfDNA, platelet- and coagulation-related markers, inflammatory markers, and intestinal perfusion assessment. Potential intervention points include nNIF-related strategies, PAD4 or GSDMD inhibition, modulation of the IP6K1/neutrophil–platelet axis, DNase-mediated degradation, enhancement of macrophage-dependent clearance, and downstream endothelial or platelet modulation.