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Human 3D Cardiac Microtissue Model to Investigate Aldosterone-Induced Fibrosis and Electrical Dysfunction.

Jacopo Burrello1, Giorgia Senesi2,3, Claudia Altomare2,3

  • 1Division of Internal Medicine and Hypertension Unit, Department of Medical Sciences (J.B., F.B., P.M., S.M.), University of Torino, Italy.

Hypertension (Dallas, Tex. : 1979)
|March 16, 2026
PubMed
Summary
This summary is machine-generated.

Aldosterone causes cardiac fibrosis and electrical changes in a novel 3D human cardiac organoid model. This preclinical model highlights the benefits of mineralocorticoid receptor antagonist therapy for primary aldosteronism patients.

Keywords:
aldosteronefibrosisorganoidspotassium

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Area of Science:

  • Cardiovascular Research
  • Organoid Technology
  • Molecular Cardiology

Background:

  • Aldosterone contributes to cardiac fibrosis and arrhythmias.
  • Preclinical models are lacking to study aldosterone-induced cardiac damage.
  • Human 3D microtissue (hMT) cardiac organoids were developed to address this gap.

Purpose of the Study:

  • To evaluate the effects of aldosterone on human 3D microtissue (hMT) cardiac organoids.
  • To investigate the molecular mechanisms of aldosterone-induced cardiac damage.
  • To assess the therapeutic potential of mineralocorticoid receptor antagonists.

Main Methods:

  • hMT were generated from human cardiac fibroblasts, endothelial cells, and cardiomyocytes.
  • Organoids were treated with aldosterone, eplerenone, and patient-derived serum.
  • Fibrosis was assessed via immunofluorescence, histology, and Western blot.
  • Electrical activity was measured using multielectrode arrays.

Main Results:

  • Patient serum with primary aldosteronism increased profibrotic markers.
  • Aldosterone induced dose-dependent fibrosis and QT interval prolongation.
  • Aldosterone downregulated KCNQ1 and ATP2A2 expression.
  • Eplerenone treatment mitigated aldosterone-induced fibrosis and electrical alterations.

Conclusions:

  • 3D hMT organoids serve as a relevant in vitro model for aldosterone-mediated cardiac effects.
  • Aldosterone directly causes cardiac fibrosis and QT prolongation in this model.
  • Findings support the role of aldosterone in cardiovascular risk and the efficacy of mineralocorticoid receptor antagonists.