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Related Experiment Video

Updated: Jun 3, 2026

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
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Published on: May 10, 2021

Circulating ACE2 levels and ACE I/D polymorphism in severe aortic stenosis.

Denisa Bianca Mercean1,2, Liviuţa Budişan3, Laura Ancuţa Pop3

  • 1Department of Morpho-functional Sciences, "Iuliu Haţieganu" University of Medicine and Pharmacy, Cluj-Napoca, 400012, Romania. MERCEAN.DENISA.BIANCA@elearn.umfcluj.ro.

Scientific Reports
|June 1, 2026
PubMed
Summary

Severe aortic stenosis (AS) is linked to higher circulating ACE2 concentrations, not ACE levels, and a distinct ACE I/D genotype distribution. This suggests an altered renin-angiotensin system balance in advanced valvular disease.

Keywords:
ACE insertion/deletion polymorphismACE2Angiotensin-converting enzymeAortic stenosisRenin–angiotensin systemValvular calcification

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09:32

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Published on: February 23, 2020

Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Biochemistry

Background:

  • The renin-angiotensin system (RAS) plays a role in the fibro-calcific remodeling seen in aortic stenosis (AS).
  • While increased angiotensin-converting enzyme 2 (ACE2) enzymatic activity is noted in severe AS, data on ACE2 protein levels and ACE genetic variations are limited.

Purpose of the Study:

  • To investigate circulating concentrations of ACE2 and ACE in severe AS patients compared to controls.
  • To examine the relationship between ACE2, ACE levels, and the ACE insertion/deletion (I/D) polymorphism in severe AS.
  • To determine if these factors are independently associated with severe AS.

Main Methods:

  • A cross-sectional case-control study involving 80 participants (40 severe AS, 40 controls).
  • Measurements of circulating ACE and ACE2 concentrations using ELISA.
  • Genotyping for the ACE I/D polymorphism (rs4340).
  • Statistical analyses included multivariable logistic regression and Firth penalized regression.

Main Results:

  • Circulating ACE2 concentrations were significantly higher in severe AS patients (median 1.9 ng/mL) versus controls (0.8 ng/mL).
  • ACE levels were comparable between groups.
  • ACE2 remained independently associated with severe AS (OR 1.48 per doubling).
  • The ACE II genotype was independently associated with severe AS compared to the ID genotype.
  • Neither ACE2 nor ACE I/D genotype correlated with stenosis severity or calcification.

Conclusions:

  • Severe AS is associated with elevated circulating ACE2 concentrations and a differential ACE I/D genotype distribution, despite similar ACE levels.
  • These findings suggest an altered systemic RAS balance in advanced valvular disease.
  • Further validation in larger prospective cohorts is warranted.