ArticleAdvanced biology2025
HMGB1 Derived from the Pyroptotic Microenvironment Promotes Macrophage Extracellular Traps in Hirschsprung-Associated Enterocolitis.
Article in Advanced biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Macrophage-enteric nervous system crosstalk in Hirschsprung disease and associated enterocolitis: a focused narrative review with clinical implications.Pediatric surgery international · 2026Review
- Review
- Involvement of the pyroptosis-HMGB1 axis in systemic diseases.Frontiers in cell and developmental biology · 2026Review
- HMGB1: a key molecule linking chronic inflammation to complications in type 2 diabetes mellitus and a target for exercise intervention.Frontiers in endocrinology · 2026Review
- HMGB1 Derived from the Pyroptotic Microenvironment Promotes Macrophage Extracellular Traps in Hirschsprung-Associated Enterocolitis.Advanced biology · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Hirschsprung-associated enterocolitis (HAEC) is the most common and severe complication in patients with Hirschsprung's disease (HSCR) and is characterized by high morbidity, frequent recurrence and substantial mortality. The formation of macrophage extracellular traps (METs), a novel inflammatory mode of cell death, plays a significant role in the progression of various inflammatory diseases. However, the mechanisms underlying METs formation and their role in the progression of HAEC remain unclear. Here, the findings indicate that METs formation induced by the pyroptotic microenvironment enhances inflammatory responses and induces colonic epithelial cells (CECs) injury in HAEC. Mechanistically, high mobility group box 1 protein (HMGB1), derived from this pyroptotic environment, mediates METs formation through toll-like receptor 4 (TLR4)-p38 MAPK/p65 NF-kB signaling pathways. Furthermore, incubation of CECs with METs induces suppression of cell viability, more production of reactive oxygen species (ROS) and pyroptosis. In conclusion, HMGB1 mediates the communication between pyroptotic microenvironment and METs formation, triggering enhanced inflammatory responses and damage to CECs. Targeting HMGB1 presents a potential therapeutic strategy for HAEC.
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