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Overexpression of human C-reactive protein exacerbates left ventricular remodeling in diabetic cardiomyopathy

Yoshinori Mano1, Toshihisa Anzai, Hidehiro Kaneko

  • 1Division of Cardiology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.

Circulation Journal : Official Journal of the Japanese Circulation Society
|April 27, 2011
PubMed

Insights

High C-reactive protein (CRP) levels worsen heart failure in diabetes. Overexpressing CRP in mice with diabetes led to severe cardiac dysfunction, inflammation, and fibrosis, highlighting CRP

Area of Science:

  • Cardiovascular Biology
  • Inflammation Research
  • Metabolic Disease Mechanisms

Background:

  • C-reactive protein (CRP) is implicated in cardiovascular pathology.
  • The specific role of CRP in heart failure, particularly in the context of diabetes, remains unclear.

Purpose of the Study:

  • To investigate the impact of human C-reactive protein (CRP) overexpression on cardiac dysfunction in a mouse model of diabetes mellitus (DM).

Main Methods:

  • Human CRP-overexpressing transgenic mice (CRP-Tg) and wild-type (Wt) mice were subjected to streptozotocin-induced diabetes.
  • Echocardiography, hemodynamic measurements, myocardial gene expression analysis, and histological assessments were performed.

Main Results:

  • CRP-Tg mice with diabetes (CRP/DM) exhibited significantly reduced cardiac function (fractional shortening, LV dP/dt max) compared to Wt mice with diabetes (Wt/DM).
  • Elevated inflammatory markers, renin-angiotensin system components, oxidative stress indicators (8-hydroxydeoxyguanosine), apoptosis markers (Bax/Bcl-2 ratio), and cardiac fibrosis were observed in CRP/DM mice.
  • Myocardial mRNA levels of key inflammatory and fibrotic mediators were increased in CRP/DM mice.

Conclusions:

  • Overexpression of human CRP significantly exacerbates left ventricular (LV) dysfunction and adverse cardiac remodeling in diabetic cardiomyopathy.
  • This exacerbation is potentially mediated by enhanced inflammation, activation of the renin-angiotensin system, and increased oxidative stress.
  • The findings suggest CRP plays a critical role in the progression of diabetic heart disease.
Abstract

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