Heritability of clot formation.
The development of occlusive arterial and venous disease is contingent on the formation of a fibrin mesh that occurs following tissue damage and activation of the coagulation system. Clinical evidence indicates that fibrin structure and function are important determinants of cardiovascular risk, and the difference between clots formed from plasma and from purified fibrinogen highlights the importance of plasma factors in determining final clot structure. Twin, family, and case-control studies indicate there is a significant genetic contribution to variance in coagulation and fibrinolytic factors that may influence clot structure. Additionally, studies indicate a smaller but significant genetic contribution to fibrin structure, with a larger component provided by the environmental contribution. Future studies of the influence of post-translational modifications to fibrin(ogen) and other factors involved in clot formation may provide important insights into thrombotic disease mechanisms.
Standeven
Kristina F
KF
Division of Cardiovascular and Diabetes Research, Multidisciplinary Cardiovascular Research Centre, University of Leeds, Leeds LS29JT, United Kingdom.
Uitte de Willige
Shirley
S
Carter
Angela M
AM
Grant
Peter J
PJ
D001777:Blood Coagulation / Q000235:genetics* / Q000502:physiology; D005176:Factor XIII / Q000235:genetics; D005340:Fibrinogen / Q000235:genetics; D005342:Fibrinolysis / Q000235:genetics; D006801:Humans; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics; D013927:Thrombosis / Q000209:etiology / Q000235:genetics*
D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D005340:Fibrinogen; D005176:Factor XIII