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Snake venoms and hemostasis
Author(s) -
LU Q.,
CLEMETSON J. M.,
CLEMETSON K. J.
Publication year - 2005
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2005.01358.x
Subject(s) - snake venom , venom , proteases , hemostasis , platelet , biochemistry , disintegrin , serine protease , coagulation , plasmin , receptor , kallikrein , chemistry , viper venoms , protease , metalloproteinase , biology , microbiology and biotechnology , enzyme , immunology , medicine
Summary. Snake venoms are complex mixtures of biologically active proteins and peptides. Many of them affect hemostasis by activating or inhibiting coagulant factors or platelets, or by disrupting endothelium. Based on sequence, these snake venom components have been classified into various families, such as serine proteases, metalloproteinases, C‐type lectins, disintegrins and phospholipases. The various members of a particular family act selectively on different blood coagulation factors, blood cells or tissues. For almost every factor involved in coagulation or fibrinolysis there is a venom protein that can activate or inactivate it. Venom proteins affect platelet function by binding or degrading vWF or platelet receptors, activating protease‐activated receptors or modulating ADP release and thromboxane A 2 formation. Some venom enzymes cleave key basement membrane components and directly affect capillary blood vessels to cause hemorrhaging. l ‐Amino acid oxidases activate platelets via H 2 O 2 production.