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In AP, early NET formation correlates with disease severity and septic complications, contributing to acinar injury, microvascular thrombosis, ductal obstruction, and organ dysfunction. In PDAC, NETs shape a fibrotic and immune-resistant tumor microenvironment by promoting stromal activation, immune exclusion, metastasis, and hypercoagulability. Tumor- and stroma-derived signals sustain NET formation within this niche. We also discuss NET-related biomarkers for risk assessment and therapy monitoring, and explore therapeutic strategies that target NETs\u2014ranging from their degradation with DNase to their inhibition of upstream pathways such as PAD4, autophagy, and oxidative signaling. Targeting NETs may also reduce their downstream effects on thrombosis and immune suppression. Overall, NETs emerge as critical drivers of pancreatic disease progression and represent promising therapeutic targets.<\/jats:p>","DOI":"10.3390\/cells15050440","type":"journal-article","created":{"date-parts":[[2026,3,2]],"date-time":"2026-03-02T16:06:59Z","timestamp":1772467619000},"page":"440","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Neutrophil Extracellular Traps in Exocrine Pancreatic Disease: A Comprehensive Review of Pathogenesis, Severity Stratification, and Therapeutic Targeting"],"prefix":"10.3390","volume":"15","author":[{"given":"Vesna","family":"Vulovic","sequence":"first","affiliation":[{"name":"Department of Surgery, University Hospital Medical Center Be\u017eanijska Kosa, 11000 Belgrade, 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