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DOI: 10.1160/TH12-07-0465
Zinc: An important cofactor in haemostasis and thrombosis
Financial support: This work was supported in part by the Canadian Institutes of Health Research (MOP 3992, MOP 102735, and CTP 79846) and the Heart and Stroke Foundation of Ontario (T4792 and T4730). T.T.V was supported by an Ontario Graduate Student of Ontario Award. J.I.W. holds the Heart and Stroke Foundation of Ontario/J. Fraser Mustard Endowed Chair in Cardiovascular Research and the Canada Research Chair (Tier 1) in Thrombosis.Publikationsverlauf
Received:
05. Juli 2012
Accepted after major revision:
27. Januar 2012
Publikationsdatum:
29. November 2017 (online)
Summary
There is mounting evidence that zinc, the second most abundant transition metal in blood, is an important mediator of haemostasis and thrombosis. Prompted by the observation that zinc deficiency is associated with bleeding and clotting abnormalities, there now is evidence that zinc serves as an effector of coagulation, anticoagulation and fibrinolysis. Zinc binds numerous plasma proteins and modulates their structure and function. Because activated platelets secrete zinc into the local microenvironment, the concentration of zinc increases in the vicinity of a thrombus. Consequently, the role of zinc varies depending on the microenvironment; a feature that endows zinc with the capacity to spatially and temporally regulate haemostasis and thrombosis. This paper reviews the mechanisms by which zinc regulates coagulation, platelet aggregation, anticoagulation and fibrinolysis and outlines how zinc serves as a ubiquitous modulator of haemostasis and thrombosis.
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