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Updated: Jul 11, 2026
06:47
Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
[Lipoprotein(a): a link between thrombogenesis and atherogenesis]
Biljana Vucković1, Mirjana Derić
1Klinicki centar Novi Sad, Novi Sad, Institut za laboratorijsku medicinu. bbvucko@eunet.yu
Medicinski Pregled
|September 15, 2007
Summary
Lipoprotein(a) [Lp(a)] acts as an independent risk factor for cardiovascular disease by interfering with the body's natural clot-dissolving mechanisms. Its structural similarity to plasminogen allows it to inhibit fibrinolysis, linking atherogenesis and thrombogenesis.
Area of Science:
- Biochemistry
- Cardiovascular Science
- Molecular Biology
Context:
- Atherosclerotic disease involves multiple thrombogenesis mechanisms.
- Lipoprotein(a) [Lp(a)], structurally similar to plasminogen, presents a pathogenic link between atherogenesis and thrombogenesis.
- Lp(a) is an independent risk factor for ischemic heart and brain diseases.
Purpose:
- To elucidate the antifibrinolytic effects of Lp(a) via apolipoprotein(a).
- To explain the molecular mechanisms by which Lp(a) influences the hemostatic system.
- To establish Lp(a) as a key factor connecting thrombogenesis and atherogenesis.
Summary:
- Lp(a) inhibits plasminogen activation and binding to receptors, thereby hindering fibrinolysis.
- Structural similarities between Lp(a) and plasminogen, including kringle domains, underlie its antifibrinolytic activity.
- Lp(a) positively correlates with plasminogen activator inhibitor-1 (PAI-1) and may promote tissue factor pathway inhibitor release.
Impact:
- Lp(a) provides a molecular explanation for the link between thrombogenesis and atherogenesis.
- Understanding Lp(a)'s role can inform strategies for managing cardiovascular risk.
- This research highlights Lp(a) as a critical target for therapeutic interventions in cardiovascular disease.
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