ABSTRACT
The hemostatic balance, introduced more than 40 years ago, addresses the components
and reactions involved in fibrin turnover. Fibrin is placed in the core of this delicate
balance. Defects in the mechanisms responsible for fibrin turnover might lead to thrombosis
or bleeding, and fibrin consequently is an important substrate in the physiology of
hemostasis.
This review describes the components and processes involved in fibrin formation and
fibrin degradation. Particular emphasis is put on the reactions involved in the conversion
of fibrinogen to fibrin, the polymerization of fibrin molecules induced by coagulation
factor XIII (FXIII), and the degradation 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 alterations 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 attention in clinical settings. Of particular importance
might be more detailed clinical studies that review the influence of polymorphisms
in the genes coding for the key factors involved in fibrin metabolism on the development
of hemostatic diseases, but also the role of elastase-induced fibrin degradation deserves
increased attention.
KEYWORD
Fibrin - coagulation - fibrinolysis - elastase - plasmin - fibrin structure - factor
XIII
