{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T13:01:06Z","timestamp":1787317266876,"version":"build-2736575974"},"reference-count":67,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T00:00:00Z","timestamp":1774915200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004281","name":"Narodowe Centrum Nauki","doi-asserted-by":"publisher","award":["The study was supported by a grant from National Science Centre, Poland (NCN) No. 2021\/43\/B\/NZ6\/00782 (EK). The open-access publication of this article was funded by the programme \u201cExcellence Initiative \u2013 Research University\u201d at the Faculty of Biology of the Jagiellonian University in Krak\u00f3w, Poland. , 2021\/43\/B\/NZ6\/00782"],"award-info":[{"award-number":["The study was supported by a grant from National Science Centre, Poland (NCN) No. 2021\/43\/B\/NZ6\/00782 (EK). The open-access publication of this article was funded by the programme \u201cExcellence Initiative \u2013 Research University\u201d at the Faculty of Biology of the Jagiellonian University in Krak\u00f3w, Poland. , 2021\/43\/B\/NZ6\/00782"]}],"id":[{"id":"10.13039\/501100004281","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Neutrophil extracellular traps (NETs) constitute a critical antimicrobial mechanism, yet excessive or dysregulated NET release contributes to endothelial injury and tissue damage. Therefore, identifying physiological and pharmacological regulators of NET formation remains an important goal. Although the role of mitochondrial dynamics in NETs remains incompletely elucidated, accumulating evidence suggests that mitochondria may be underexplored regulators with therapeutic potential. In fact, in certain NET forms, their DNA is of mitochondrial origin. Here, we investigated how exogenous dimethyl fumarate (DMF), an ester of the tricarboxylic acid cycle (TCA) metabolite fumarate, modulates NET formation. Foremost, we observed that DMF markedly suppresses PAD4-dependent NET release by LPS-stimulated neutrophils of wild-type and PAD4-deficient mice. Mechanistic analyses demonstrated that DMF activates the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway and increases the secretion of anti-inflammatory Annexin A1 (ANXA1). Functionally, inhibition of either Nrf2 or the ANXA1 receptor Fpr2 restores NET formation. To integrate these observations with mitochondrial function, we examined markers of mitochondrial dynamics. We found that DMF decreases phosphorylation of dynamin-related protein 1 (DRP1) at Serine 616, a modification typically associated with reduced mitochondrial fission. Consistently, pharmacological inhibition of DRP1 (Mdivi-1) also diminishes NET formation, whereas induction of mitochondrial fragmentation (CCCP) triggers PANoptotic neutrophil death and extracellular DNA release, both of which were prevented by DMF. Collectively, these data identify DMF as a mitochondria-linked immunometabolic regulator that suppresses NET formation through coordinated engagement of Nrf2 and ANXA1 signaling and modulation of mitochondrial dynamics. These findings highlight mitochondrial remodeling as a promising avenue for future exploration and position DMF as a potential pharmacological tool for controlling excessive neutrophil activation.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1770063","type":"journal-article","created":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T04:12:56Z","timestamp":1774930376000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Fumarate inhibits the formation of neutrophil extracellular traps (NETs) in a Nrf2-controlled and Annexin-A1-dependent manner associated with mitochondrial fusion"],"prefix":"10.3389","volume":"17","author":[{"given":"Gabriela","family":"Burczyk","sequence":"first","affiliation":[{"name":"Department of Experimental Hematology, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University","place":["Krakow, Poland"]},{"name":"Doctoral School of Exact and Natural Sciences, Faculty of Biology, Jagiellonian University","place":["Krakow, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elzbieta","family":"Kolaczkowska","sequence":"additional","affiliation":[{"name":"Department of Experimental Hematology, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University","place":["Krakow, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,31]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"395","DOI":"10.1038\/s41418-018-0261-x","article-title":"To NET or not to NET:current opinions and state of the science regarding the formation of neutrophil extracellular traps","volume":"26","author":"Boeltz","year":"2019","journal-title":"Cell Death Differ"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1092385","article-title":"Neutrophil Extracellular Traps Kill 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