Lipoprotein (a) in the regulation of fibrinolysis.

Published

Journal Article (Review)

Elevated plasma levels of lipoprotein(a) [LP(a)] are associated with increased an risk of developing atherosclerosis. This increased risk may be due to an Lp(a)-mediated depression of fibrinolytic activity. Lp(a) regulates fibrinolysis by controlling the activity of plasminogen activators. Lp(a) is a low density lipoprotein with an apoprotein(a) subunit which has a high degree of homology with the fibrinolytic zymogen plasminogen. The apoprotein(a) subunit contains up to thirty seven copies of a domain homologous to the plasminogen kringle 4 domain, which enables Lp(a) to bind to fibrin. The subunit also has a zymogen domain, but it is not activated by plasminogen activators. Lp(a) inhibits plasminogen activation by competing with plasminogen for access to plasminogen activators bound to vascular surfaces. Lp(a) also competes with the irreversible inhibitor of plasminogen activators, plasminogen activator inhibitor-1. Therefore increases in Lp(a) concentration may decrease fibrinolytic activity by preventing activation of plasminogen, but Lp(a) may also prolong plasminogen activation by preventing the irreversible inhibition of the activators. At elevated levels of Lp(a) the decreased rate of plasmin generation may not be offset by the prolongation in plasminogen activation, and fibrinolysis will be inhibited.

Full Text

Duke Authors

Cited Authors

  • Edelberg, JM; Pizzo, SV

Published Date

  • 1995

Published In

Volume / Issue

  • 2 Suppl 1 /

Start / End Page

  • S5 - S7

PubMed ID

  • 9225222

Pubmed Central ID

  • 9225222

International Standard Serial Number (ISSN)

  • 1340-3478

Digital Object Identifier (DOI)

  • 10.5551/jat1994.2.supplement1_s5

Language

  • eng

Conference Location

  • Japan