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Factor XII in inflammation and wound healing

Stavrou, Evi X.a,b

doi: 10.1097/MOH.0000000000000450
HEMOSTASIS AND THROMBOSIS: Edited by Alvin H. Schmaier

Purpose of review This review describes the contribution of coagulation factor XII (FXII) in sterile inflammation and wound healing, focusing on recently identified roles for zymogen FXII in neutrophil functions.

Recent findings Recent studies have identified an important role for FXII in neutrophil trafficking. In particular, following neutrophil activation, autocrine FXII signals through the urokinase plasminogen activator receptor (uPAR) on the neutrophil surface to upregulate neutrophil functions. The sum of these activities leads to neutrophil adhesion, chemotaxis, and neutrophil extracellular (NET) formation. Downregulating FXII-mediated signaling in neutrophils is associated with improved wound healing.

Summary These recent findings show the sophisticated role of FXII in vivo and create new opportunities for research on the treatment of chronic inflammatory diseases.

aDepartment of Medicine, Louis Stokes Veterans Administration Medical Center

bDepartment of Medicine, Hematology and Oncology Division, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA

Correspondence to Evi X. Stavrou, MD, Department of Medicine, Hematology and Oncology Division, Case Western Reserve University School of Medicine, 2143 WRB, 2103 Cornell Road, Cleveland, OH 44106, USA. Tel: +1 216 368 6986; fax: +1 216 368 1166; e-mail: evi.stavrou@case.edu

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