Abstract
Besides mediating hemostatic functions, platelets are increasingly recognized as important players of inflammation. Data from experiments in mice and men revealed various intersection points between thrombosis, hemostasis, and inflammation, which are addressed and discussed in this review in detail. One such example is the intrinsic coagulation cascade that is initiated after platelet activation thereby further propagating and re-enforcing wound healing or thrombus formation but also contributing to the pathophysiology of severe diseases. FXII of the intrinsic pathway connects platelet activation with the coagulation cascade during immune reactions. It can activate the contact system thereby either creating an inflammatory state or accelerating inflammation. Recent insights into platelet biology could show that platelets are equipped with complement receptors. Platelets are important for tissue remodeling after injury has been inflicted to the endothelial barrier and to the subendothelial tissue. Thus, platelets are increasingly recognized as more than just cells relevant for bleeding arrest. Future insights into platelet biology are to be expected. This research will potentially offer novel opportunities for therapeutic intervention in diseases featuring platelet abundance.
Highlights
In recent years, an increasing body of evidence demonstrates that platelets have several functions beyond hemostasis [1, 2]
Platelets contribute to vascular inflammation of the brain during stroke or experimental autoimmune encephalitis (EAE) [2, 3]
The inflammatory cytokine IL-6 was shown to be linked to increased plasma levels of thrombopoietin and an increased platelet number in a murine and human setting [17] and TPO was shown to augment platelet P-selectin (CD62P) expression stimulating platelet-leukocyte associations [18]
Summary
Matthias Mezger 1, Henry Nording 1,2, Reinhard Sauter 1, Tobias Graf 1, Christian Heim 3, Nikolas von Bubnoff 4, Stephan M. Data from experiments in mice and men revealed various intersection points between thrombosis, hemostasis, and inflammation, which are addressed and discussed in this review in detail. One such example is the intrinsic coagulation cascade that is initiated after platelet activation thereby further propagating and re-enforcing wound healing or thrombus formation and contributing to the pathophysiology of severe diseases. FXII of the intrinsic pathway connects platelet activation with the coagulation cascade during immune reactions. It can activate the contact system thereby either creating an inflammatory state or accelerating inflammation.
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