Fibrin clot formation and lysis: Basic mechanisms

Citation
Jj. Sidelmann et al., Fibrin clot formation and lysis: Basic mechanisms, SEM THROMB, 26(6), 2000, pp. 605-618
Citations number
136
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
SEMINARS IN THROMBOSIS AND HEMOSTASIS
ISSN journal
00946176 → ACNP
Volume
26
Issue
6
Year of publication
2000
Pages
605 - 618
Database
ISI
SICI code
0094-6176(2000)26:6<605:FCFALB>2.0.ZU;2-2
Abstract
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.