Tissue factor as a link between inflammation and coagulation

Due to its receptor activity for factor VII, tissue factor (TF) is primary initiator of the blood coagulation cascade and ensures rapid hemostasis in case of organ damage. Inflammatory cytokines, such as tumor necrosis factor-α or interleukins, strongly induce expression of both full-length TF as we...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Trends in cardiovascular medicine Jg. 26; H. 4; S. 297 - 303
Hauptverfasser: Witkowski, Marco, Landmesser, Ulf, Rauch, Ursula
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Elsevier Inc 01.05.2016
Elsevier Limited
Schlagworte:
Acute coronary syndromes
Alternative Splicing
Angiogenesis
Animals
Blood clots
Blood Coagulation
Cancer
Cardiovascular
Coagulation
Diabetes
Endothelium
Gene Expression Regulation
Homeostasis
Humans
Inflammation
Inflammation - blood
Inflammation - genetics
Inflammation Mediators - blood
Protein Conformation
Protein folding
Signal Transduction
Thromboplastin - chemistry
Thromboplastin - genetics
Thromboplastin - metabolism
Thrombosis
Tissue factor
Vessel
Vessel
Inflammation
Tissue factor
Coagulation
Endothelium
Tissue Factor
ISSN:1050-1738, 1873-2615, 1873-2615
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Due to its receptor activity for factor VII, tissue factor (TF) is primary initiator of the blood coagulation cascade and ensures rapid hemostasis in case of organ damage. Inflammatory cytokines, such as tumor necrosis factor-α or interleukins, strongly induce expression of both full-length TF as well as the alternatively spliced TF in endothelial and blood cells. Beyond its role in hemostasis, TF also has signaling activity and promotes pleiotropic inflammatory responses via protease-activated receptors in concert with other coagulation factors. Alteration of TF expression and TF alternative splicing provides an effective means to change the endothelial phenotype and modulate inflammatory responses of the vessel.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
ISSN:1050-1738
1873-2615
1873-2615
DOI:10.1016/j.tcm.2015.12.001