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Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
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Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

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Blockage of receptor for advanced glycation end products prevents development of cardiac dysfunction in db/db type 2

Jan M Nielsen1, Steen B Kristiansen, Rikke Nørregaard

  • 1Department of Cardiology, Aarhus University Hospital, Skejby, 8200 Aarhus N, Denmark. janmn@dadlnet.dk

European Journal of Heart Failure
|June 9, 2009
PubMed
Abstract

Insights

Activation of the receptor for advanced glycation end products (RAGE) contributes to cardiac dysfunction in type 2 diabetes. Blocking RAGE improved systolic function and reduced myocardial stiffness in diabetic mice.

Area of Science:

  • Cardiovascular Research
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Receptor for advanced glycation end products (RAGE) activation is linked to diabetes complications.
  • Cardiac dysfunction is a common long-term complication in diabetes mellitus.

Purpose of the Study:

  • To investigate the role of RAGE activation in the diabetic myocardium.
  • To determine if blocking RAGE signaling can prevent or reverse cardiac dysfunction in type 2 diabetes.

Main Methods:

  • Utilized a type 2 diabetic mouse model (db/db) for cardiac function assessment.
  • Employed MRI and conductance catheter techniques to evaluate cardiac performance.
  • Assessed the impact of RAGE antibody treatment on cardiac function and gene expression.

Main Results:

  • Diabetic mice exhibited accelerated age-dependent cardiac dysfunction.
  • RAGE blockade preserved systolic function and reduced left ventricular diastolic stiffness.
  • RAGE inhibition decreased collagen expression and normalized myosin isoform expression in the myocardium.

Conclusions:

  • RAGE activation is a key pathogenic mechanism in diabetic cardiac dysfunction.
  • Mechanisms involve alterations in myocardial biophysical properties and myocyte function.
  • Targeting RAGE may offer therapeutic potential for diabetic heart disease.

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