Sara Baratchi

Conflicts of Interest The authors declare no conflicts of interest. References 1, , , et al., “Innate-Adaptive Immunity Interplay and Redox Regulation in Immune Response,” Redox Biology 37 (2020): 101759. 2, , and , “Editorial: Danger Signals Triggering Immune Response and Inflammation,” Frontiers in Immunology 8 (2017): 979. 3 and , “Neutrophil Extracellular Traps: Double-Edged Swords of Innate Immunity,” Journal of Immunology 189 (2012): 2689–2695.

Abstract Neutrophil infiltration and subsequent extracellular trap formation (NETosis) is a contributing factor in sterile inflammation. Furthermore, neutrophil extracellular traps (NETs) are prothrombotic, as they provide a scaffold for platelets and red blood cells to attach to. In circulation, neutrophils are constantly exposed to hemodynamic forces such as shear stress, which in turn regulates many of their biological functions such as crawling and NETosis.

Originally published8 Jul 2020https://doi.org/10.1161/CIRCULATIONAHA.120.045536Circulation. ;0 Abstract Background: Aortic valve stenosis is an increasingly prevalent degenerative and inflammatory disease. Transcatheter aortic valve implantation (TAVI) has revolutionized its treatment, thereby avoiding its life-threatening/disabling consequences. Whether aortic valve stenosis is accelerated by inflammation and whether it is itself a cause of inflammation are unclear.