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Iron-induced fibrin in cardiovascular disease

Boguslaw Lipinski1, Etheresia Pretorius

  • 1Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.

Current Neurovascular Research
|June 1, 2013
PubMed

Insights

Excessive iron in blood can cause fibrinogen to form resistant clots, promoting chronic inflammation and cardiovascular disease (CVD). Iron chelators and radical scavengers may prevent these harmful deposits.

Area of Science:

  • Biochemistry
  • Pathology
  • Cardiovascular Science

Background:

  • Cardiovascular disease (CVD) is linked to chronic inflammation.
  • Fibrin clots are normally degraded by the fibrinolytic system.
  • Fibrinolytic therapy for thrombosis has a narrow time window for effectiveness.

Purpose of the Study:

  • To investigate the role of iron in fibrinogen polymerization and clot resistance.
  • To explore the link between persistent fibrin clots and chronic inflammation.
  • To evaluate potential interventions against iron-induced clot formation.

Main Methods:

  • Studied iron (FeIII)-induced conversion of fibrinogen to para-fibrin.
  • Utilized scanning electron microscopy to visualize polymerization.
  • Investigated effects of amphiphilic substances on iron- and thrombin-induced polymerization.

Main Results:

  • Trivalent iron (FeIII) promotes formation of fibrin-like polymers (parafibrin) resistant to degradation.
  • Excessive free iron accumulation in blood is associated with CVD.
  • Persistent, proteolysis-resistant fibrin clots are suggested to cause chronic inflammation.

Conclusions:

  • Excessive iron accumulation in blood may drive the formation of persistent, pro-inflammatory fibrin clots.
  • Iron chelating agents are proposed as a method to prevent iron overload.
  • Free radical scavengers warrant investigation for preventing fibrin-like deposits and associated diseases.

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