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ACE2 and diabetic complications.

Rachael G Dean1, Louise M Burrell

  • 1Department of Medicine, University of Melbourne, Austin Health, Heidelberg 3081, Victoria, Australia.

Current Pharmaceutical Design
|September 28, 2007
PubMed
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The renin-angiotensin system (RAS) enzyme ACE2 counter-regulates ACE, impacting diabetic complications. Targeting ACE2 offers potential for novel diabetes treatments.

Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Nephrology

Background:

  • The renin-angiotensin system (RAS) plays a crucial role in cardiovascular and renal function.
  • Angiotensin converting enzyme (ACE) converts Angiotensin I to Angiotensin II, a key mediator of RAS effects.
  • The discovery of ACE2, which degrades Angiotensin II and produces Angiotensin 1-7, has added complexity to the classical RAS view.

Purpose of the Study:

  • To review the current understanding of ACE2's role in the pathophysiology of diabetic complications.
  • To explore the potential of targeting ACE2 for therapeutic interventions in diabetes.

Main Methods:

  • Literature review of studies investigating ACE2 in the context of diabetes.
  • Analysis of the counter-regulatory balance between ACE and ACE2 in the heart and kidney.

Related Experiment Videos

  • Discussion of the implications of ACE2 activity in microvascular and macrovascular complications of diabetes.

    • Main Results:

    • ACE2 is present in the heart and kidney, suggesting a role in these organs.
    • ACE2 is believed to act counter-regulatory to ACE, modulating vasoconstrictor and vasodilator balance.
    • Activation of the RAS contributes significantly to diabetic complications, and ACE inhibition alone is insufficient.

    Conclusions:

    • ACE2 plays a significant role in cardiac and renal pathophysiology, particularly in diabetes.
    • Targeting ACE2 presents a novel therapeutic opportunity for preventing and treating diabetic complications.
    • Further research into ACE2's function in diabetes is warranted to develop specific modulators.