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Asselbergs, F.W. et al.

Folkert W. Asselbergs, Kristine Pattin, Harold Snieder, Hans L. Hillege, Wiek H. van Gilst, Jason H. Moore,

Genetic architecture of tissue-type plasminogen activator and plasminogen activator inhibitor-1.

Important biochemical constituents of the fibrinolytic system include tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1). In the current review, we aim to describe the genetic architecture of t-PA and PAI-1. Several genetic polymorphisms in the T-PA and PAI-1 gene have been found to be associated with t-PA and PAI-1 levels in different patient cohorts. However, these genetic variations explain only a minor part of the heritability of t-PA and PAI-1, suggesting that genes in other pathways may influence t-PA and PAI-1 levels, and that epistasis and gene-environment interactions may play an important role in determining plasma levels of t-PA and PAI-1. Several studies reported that interindividual variation in plasma levels of t-PA and PAI-1 are significantly influenced by common polymorphisms in genes from the renin-angiotensin and bradykinin systems. In addition, we and others documented several gene-environment interactions and epistatic effects of genetic polymorphisms in the renin-angiotensin, bradykinin, and fibrinolytic systems on plasma t-PA and PAI-1 levels. In future studies, we need to consider high-order interactions and additional polymorphisms in genes from other (unknown) pathways detected by genome-wide association studies to fully understand the complex genetic architecture of these important intermediate quantitative traits and thereby thrombosis.[1]

References

Genetic architecture of tissue-type plasminogen activator and plasminogen activator inhibitor-1. Asselbergs, F.W., Pattin, K., Snieder, H., Hillege, H.L., van Gilst, W.H., Moore, J.H. Semin. Thromb. Hemost. (2008) [Pubmed]

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