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Novel pathways and therapies in experimental diabetic atherosclerosis

Christine Koulis1, Judy B de Haan, Terri J Allen

  • 1Diabetic Complications Group, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia.

Expert Review of Cardiovascular Therapy
|March 7, 2012
PubMed

Insights

Diabetic vascular complications arise from specific molecular pathways. Targeting the advanced glycation end product/receptor for advanced glycation end product (AGE/RAGE) axis and related pathways may offer novel therapeutic strategies.

Area of Science:

  • Vascular biology
  • Endocrinology
  • Molecular medicine

Background:

  • Diabetes mellitus significantly increases the risk of major vascular complications.
  • Existing treatments improve glycemic and blood pressure control but often fail to prevent diabetes-mediated macrovascular disease.

Purpose of the Study:

  • To review key molecular pathways implicated in diabetic vascular injury.
  • To highlight the role of the AGE/RAGE axis, HMGB1, renin-angiotensin system, urotensin II, PPAR, inflammation, and oxidative stress.

Main Methods:

  • Literature review focusing on molecular mechanisms of diabetic vascular complications.
  • Analysis of the interplay between AGE/RAGE axis and HMGB1.
  • Examination of evidence for other contributing pathways.

Main Results:

  • The advanced glycation end product/receptor for advanced glycation end product (AGE/RAGE) axis and its interaction with HMGB1 are central to diabetic vascular injury.
  • The renin-angiotensin system, urotensin II, PPAR, inflammation, and oxidative stress also play significant roles.

Conclusions:

  • Understanding these specific pathways is crucial for developing effective treatments.
  • Targeting these pathways offers potential for novel therapies to mitigate diabetic vascular complications.

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