{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T08:11:03Z","timestamp":1791360663732,"version":"4.3.1"},"reference-count":39,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T00:00:00Z","timestamp":1756944000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["GNT2020197"],"award-info":[{"award-number":["GNT2020197"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["GNT2033680"],"award-info":[{"award-number":["GNT2033680"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["BioEssays"],"published-print":{"date-parts":[[2025,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Neutrophil extracellular traps (NETs)\u2014web\u2010like DNA structures extruded by neutrophils in response to various stimuli, including pathogens, sterile inflammation, and mechanical stress\u2014play a dual role in immunity and disease. While NETs serve to trap and neutralize pathogens during host defense, excessive or dysregulated NET formation, known as NETosis, can amplify inflammation and contribute to thrombotic complications such as atherosclerosis and valve disease. Increasing evidence supports that NETosis is a regulated, signaling\u2010driven process, and that mechanical forces\u2014including shear stress, tensile force, and matrix stiffness\u2014can act as noncanonical danger signals capable of inducing NETosis. Mechanosensitive ion channels such as Piezo1, have emerged as key transducers of these biophysical cues, enabling cells to convert changes in shear stress levels into intracellular calcium flux, cytoskeletal remodeling, and ultimately NET release. Furthermore, exposure to pathologically high levels of shear stress may improve the sensitivity of neutrophils to secondary stimuli, lowering their activation threshold and amplifying inflammatory and thrombotic cascades. This mechanosensitive framework highlights shear\u2010induced NETosis as a critical pathway by which neutrophils contribute to inflammation and thrombosis in mechanically stressed vascular environments.<\/jats:p>","DOI":"10.1002\/bies.70065","type":"journal-article","created":{"date-parts":[[2025,9,5]],"date-time":"2025-09-05T06:55:56Z","timestamp":1757055356000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Shear Stress as a Danger Signal: Inducing Inflammation and Thrombosis via Mechanosensitive NETosis"],"prefix":"10.1002","volume":"47","author":[{"given":"Sara","family":"Baratchi","sequence":"first","affiliation":[{"name":"Baker Heart and Diabetes Institute  Melbourne Victoria Australia"},{"name":"Department of Cardiometabolic Health University of Melbourne  Parkville Victoria Australia"},{"name":"School of Health and Biomedical Sciences RMIT University  Melbourne Victoria 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