• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

Factor VII activating protease deficiency promotes neointima formation by enhancing leukocyte accumulation
ConclusionsFSAP deficiency causes an increase in CCL2 expression and CCL2‐mediated infiltration of leukocytes into the injured vessel, thereby promoting SMC proliferation and migration by activation of leukocyte‐derived gelatinases. These results provide a possible explanation for the observed association of the loss‐of‐function MI‐SNP with vascular proliferative diseases.This article is protected by copyright. All rights reserved.
Source: Journal of Thrombosis and Haemostasis - July 18, 2016 Category: Hematology Authors: Jan‐Marcus Daniel, Christoph A. Reichel, Thomas Schmidt‐Woell, Jochen Dutzmann, Gabriele Zuchtriegel, Fritz Krombach, Joerg Herold, Johann Bauersachs, Daniel G. Sedding, Sandip M. Kanse Tags: Original Article ‐ Vascular Biology Source Type: research

Factor VII activating protease deficiency promotes neointima formation by enhancing leukocyte accumulation.
CONCLUSIONS: FSAP deficiency causes an increase in CCL2 expression and CCL2-mediated infiltration of leukocytes into the injured vessel, thereby promoting SMC proliferation and migration by activation of leukocyte-derived gelatinases. These results provide a possible explanation for the observed association of the loss-of-function MI-SNP with vascular proliferative diseases. This article is protected by copyright. All rights reserved. PMID: 27431088 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - July 18, 2016 Category: Hematology Authors: Daniel JM, Reichel CA, Schmidt-Woell T, Dutzmann J, Zuchtriegel G, Krombach F, Herold J, Bauersachs J, Sedding DG, Kanse SM Tags: J Thromb Haemost Source Type: research

Factor VII ‐activating protease deficiency promotes neointima formation by enhancing leukocyte accumulation
ConclusionsFSAP deficiency causes an increase in CCL2 expression and CCL2‐mediated infiltration of leukocytes into the injured vessel, thereby promoting SMC proliferation and migration by the activation of leukocyte‐derived gelatinases. These results provide a possible explanation for the observed association of the loss‐of‐function MI‐SNP with vascular proliferative diseases.
Source: Journal of Thrombosis and Haemostasis - September 6, 2016 Category: Hematology Authors: J. ‐M. Daniel, C. A. Reichel, T. Schmidt‐Woell, J. Dutzmann, G. Zuchtriegel, F. Krombach, J. Herold, J. Bauersachs, D. G. Sedding, S. M. Kanse Tags: Original Article Source Type: research