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Annexin A5 in cardiovascular disease and systemic lupus erythematosus

Anna Cederholm1, Johan Frostegård

  • 1Center for Infectious Medicine and Unit of Rheumatology, F59, Department of Medicine, Karolinska University Hospital, Huddinge, S-141 86 Stockholm, Sweden. anna.cederholm@medhs.ki.se

Immunobiology
|December 6, 2005
PubMed

Insights

Systemic lupus erythematosus (SLE) patients with cardiovascular disease (CVD) show impaired Annexin A5 (ANXA5) binding to endothelium. This dysfunction, linked to antiphospholipid antibodies (aPL), suggests ANXA5

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Rheumatology

Background:

  • Atherosclerosis, a leading cause of cardiovascular disease (CVD) mortality, is an inflammatory condition.
  • Systemic lupus erythematosus (SLE) patients exhibit a significantly elevated risk of CVD.
  • Antiphospholipid antibodies (aPL) are implicated in the heightened CVD risk observed in SLE patients.

Purpose of the Study:

  • To explore the potential role of Annexin A5 (ANXA5) in the pathogenesis of CVD, particularly in the context of atherosclerosis and atherothrombosis.
  • To investigate the impact of SLE-associated antiphospholipid antibodies (aPL) on ANXA5 function in relation to cardiovascular health.

Main Methods:

  • Review of existing literature on atherosclerosis, SLE, antiphospholipid antibodies (aPL), and Annexin A5 (ANXA5).
  • Analysis of ANXA5's known antithrombotic properties and its interaction with cell surfaces.
  • Examination of studies linking aPL interference with ANXA5 binding to adverse outcomes in SLE and its potential relevance to CVD.

Main Results:

  • Annexin A5 (ANXA5) possesses antithrombotic properties by shielding thrombogenic cell surfaces.
  • Antiphospholipid antibodies (aPL) in SLE patients interfere with ANXA5 binding to placental trophoblasts, contributing to microthrombosis and miscarriage.
  • ANXA5 is abundant in advanced atherosclerotic lesions, and sera from SLE patients with CVD inhibit ANXA5 binding to endothelium, mediated by aPL.

Conclusions:

  • Annexin A5 (ANXA5) may play a critical role in the development of cardiovascular disease (CVD) in patients with systemic lupus erythematosus (SLE).
  • The interference of antiphospholipid antibodies (aPL) with ANXA5 function is a potential mechanism linking SLE to accelerated atherosclerosis and atherothrombosis.
  • Further research into ANXA5's involvement could reveal novel therapeutic targets for managing CVD risk in SLE patients.

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