The hemostatic balance, introduced more than 40 years ago, addresses the co
mponents and reactions involved in fibrin turnover. Fibrin is placed in the
core of this delicate balance. Defects in the mechanisms responsible for f
ibrin turnover might lead to thrombosis or bleeding, and fibrin consequentl
y is an important substrate in the physiology of hemostasis.
This review describes the components and processes involved in fibrin forma
tion and fibrin degradation. Particular emphasis is put on the reactions in
volved in the conversion of fibrinogen to fibrin, the polymerization of fib
rin molecules induced by coagulation factor XIII (FXIII), and the degradati
on of fibrinogen and fibrin mediated by plasmin and elastase. Furthermore,
factors influencing fibrin structure and fibrin breakdown are addressed; in
particular polymorphisms in the genes coding for fibrinogen and FXIII, but
also the physical and biochemical conditions in which fibrin is formed.
The past decades have produced a bulk of biochemical publications reviewing
fibrin turnover and fibrin structure, and it has been shown that alteratio
ns in fibrin structure are important for the development of various disease
conditions, whereas, the architecture of fibrin can be modified by certain
drugs and chemical compounds. However, these topics deserve increased atte
ntion in clinical settings. Of particular importance might be more detailed
clinical studies that review the influence of polymorphisms in the genes c
oding for the key factors involved in fibrin metabolism on the development
of hemostatic diseases, but also the role of elastase-induced fibrin degrad
ation deserves increased attention.