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Related Experiment Video

Updated: May 31, 2026

Echocardiographic Assessment of the Right Heart in Mice
09:29

Echocardiographic Assessment of the Right Heart in Mice

Published on: November 27, 2013

ACE2 improves right ventricular function in a pressure overload model.

Jennifer A Johnson1, James West, Karen B Maynard

  • 1Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America. jennifer.johnson.2@vanderbilt.edu

Plos One
|June 23, 2011
PubMed
Summary
This summary is machine-generated.

Recombinant human angiotensin-converting enzyme 2 (rhACE2) improved right ventricular (RV) function and reduced hypertrophy in a mouse model of pulmonary hypertension. This suggests rhACE2 may be a novel therapeutic for RV failure.

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Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
10:18

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model

Published on: June 29, 2014

Area of Science:

  • Cardiovascular Research
  • Pulmonary Hypertension
  • Heart Failure

Background:

  • Right ventricular (RV) dysfunction is a significant complication of pulmonary hypertension, associated with poor prognosis.
  • Current pharmacological therapies aim to improve RV function, reduce symptoms, and enhance survival in pulmonary hypertension.
  • The study investigates the potential of recombinant human angiotensin-converting enzyme 2 (rhACE2) to improve RV function in a pressure overload model.

Purpose of the Study:

  • To evaluate the efficacy of rhACE2 in improving RV systolic and diastolic function.
  • To assess the impact of rhACE2 on RV hypertrophy and cardiac fibrosis.
  • To explore the effects of rhACE2 on Mas receptor and connexin 37 expression in the context of RV pressure overload.

Main Methods:

  • Utilized a mouse model of pulmonary artery banding to induce RV pressure overload.
  • Administered rhACE2 at a dose of 1.8 mg/kg/day.
  • Assessed RV function using in vivo hemodynamics, including ejection fraction and end-diastolic pressure.
  • Quantified RV hypertrophy via RV/LV+S ratio and evaluated fibrosis using trichrome staining and collagen1α1 expression.

Main Results:

  • rhACE2 administration significantly improved RV systolic and diastolic function, increasing RV ejection fraction and decreasing RV end-diastolic pressure.
  • rhACE2 treatment led to a significant reduction in RV hypertrophy.
  • No adverse effects on left ventricular (LV) function or significant changes in fibrosis were observed; however, Mas receptor expression increased and connexin 37 expression was normalized.

Conclusions:

  • rhACE2 effectively diminished RV hypertrophy and improved both systolic and diastolic function in a mouse model of RV pressure overload.
  • The observed improvements were associated with changes in intercellular communication markers.
  • rhACE2 presents a potential novel therapeutic strategy for managing RV failure.