{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T11:08:38Z","timestamp":1785409718986,"version":"3.56.0"},"reference-count":168,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T00:00:00Z","timestamp":1785369600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Obesity-driven type 2 diabetes mellitus is sustained by chronic low-grade sterile inflammation. The intercellular mechanisms underlying this self-amplifying state remain incompletely defined. Extracellular vesicles and neutrophil extracellular traps have each been independently implicated in metabolic inflammation. Whether they form a coordinated pathological axis in the obesity\/type 2 diabetes microenvironment has not been systematically synthesized. This narrative review integrates current mechanistic evidence in three areas: vesicle biogenesis and cargo remodeling in obesity; trap formation in the hyperglycemic and hyperlipidemic milieu; and molecular cross-talk between the two systems. We attend explicitly to the level of clinical evidence supporting each step. Our central argument is the following. Adipocyte- and macrophage-derived vesicles enriched in pro-inflammatory microRNAs activate neutrophils to undergo NETosis. The resulting traps release damage-associated molecules. These molecules stimulate further vesicle secretion. A self-reinforcing positive feedback circuit emerges. It operates through Toll-like receptor signaling, the NLRP3 inflammasome, peptidylarginine deiminase 4, and the cyclic GMP-AMP synthase\u2013stimulator of interferon genes axis. The vesicle pool in obesity is not uniformly pathogenic. Insulin-sensitizing populations also exist. Hepatocyte exosomes from early-onset obese mice are enriched in microRNA-3075 and improve insulin sensitivity. Small vesicles from rosiglitazone-treated adipose tissue macrophages are enriched in microRNA-690 and exert similar effects. Any therapeutic strategy must preserve these protective populations. The pathogenic arm propagates local adipose inflammation systemically. This drives insulin resistance, pancreatic \u03b2-cell injury, hepatic inflammation, and the vascular, renal, and ocular complications of diabetes. Preclinical interruption of the circuit shows multi-organ benefit. Candidate strategies include peptidylarginine deiminase 4 inhibition, DNase I, NLRP3 blockade, and engineered therapeutic vesicles. Among clinically deployed agents, metformin and sodium\u2013glucose cotransporter 2 inhibitors already show anti-trap and anti-inflammasome activity. The framework is mechanistically compelling. The evidence base, however, remains predominantly preclinical. No completed randomized controlled trial in obesity-related type 2 diabetes has yet validated it. Translation requires multidisciplinary collaboration, methodological standardization, sex-stratified design, and adequately powered prospective human studies.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1865003","type":"journal-article","created":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T10:49:10Z","timestamp":1785408550000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Mechanistic interplay between extracellular vesicles and neutrophil extracellular traps: unveiling the \u201csterile inflammation\u201d cascade in obesity-induced diabetes progression"],"prefix":"10.3389","volume":"17","author":[{"given":"He","family":"Gao","sequence":"first","affiliation":[{"name":"Liaoning University of Traditional Chinese Medicine","place":["Shenyang, China"]},{"name":"The First Affiliated Hospital of Liaoning University of Traditional Chinese Medicine","place":["Shenyang, 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