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Updated: Jun 5, 2026

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
07:13

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure

Published on: April 30, 2020

C-reactive protein overexpression exacerbates pressure overload-induced cardiac remodeling through enhanced

Toshiyuki Nagai1, Toshihisa Anzai, Hidehiro Kaneko

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

Hypertension (Dallas, Tex. : 1979)
|January 12, 2011
PubMed

Insights

Elevated C-reactive protein (CRP) contributes to heart failure development by worsening cardiac remodeling, inflammation, and oxidative stress in pressure overload models. This suggests CRP has a direct pathogenic role in heart disease progression.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Serum C-reactive protein (CRP) elevation is a known predictor of heart failure in hypertensive patients.
  • CRP is implicated in activating macrophages and increasing oxidative stress, key factors in cardiovascular disease.

Purpose of the Study:

  • To investigate the direct pathogenic role of CRP in pressure overload-induced cardiac remodeling.
  • To elucidate the mechanisms by which CRP influences cardiac inflammation and oxidative stress.

Main Methods:

  • Utilized transgenic mice overexpressing human CRP (CRPtg) and wild-type littermates (CON).
  • Subjected mice to transverse aortic constriction (TAC) or sham operation to induce pressure overload.
  • Analyzed myocardial gene/protein expression, macrophage infiltration, NF-κB activation, reactive oxygen species (ROS), fibrosis, and cardiac function.

Main Results:

  • TAC/CRPtg mice exhibited significantly increased myocardial inflammation (IL-6, CD68), oxidative stress markers (GPx3, p47(phox), ROS), and fibrosis compared to TAC/CON mice.
  • CRP overexpression exacerbated cardiac hypertrophy, fibrosis, and diastolic dysfunction (increased LV end-diastolic pressure, decreased fractional shortening) post-TAC.
  • Elevated angiotensin type 1 receptor, TGF-β1, and inflammatory markers were observed in TAC/CRPtg hearts.

Conclusions:

  • CRP itself plays a pathogenic role in pressure overload-induced cardiac remodeling.
  • CRP exacerbates cardiac dysfunction and fibrosis, likely mediated by enhanced inflammation and oxidative stress.
  • These findings highlight CRP as a potential therapeutic target for preventing heart failure progression.

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