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Related Experiment Video

Updated: May 13, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

Vascular calcification--is aldosterone a culprit?

Florian Lang¹, Eberhard Ritz, Jakob Voelkl

¹Department of Physiology, University of Tübingen, Tübingen, Germany. florian.lang@uni-tuebingen.de

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association

|March 12, 2013

Summary

High phosphate levels and aldosterone contribute to vascular calcification in chronic kidney disease (CKD). Spironolactone, a mineralocorticoid receptor antagonist, reversed these detrimental osteoinductive processes in mice and human cells.

Keywords:

chronic kidney disease klotho mineralocorticoid receptor osteoinductive signalling spironolactone

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A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro

Published on: June 2, 2022

Area of Science:

Nephrology
Cardiovascular Medicine
Molecular Biology

Background:

Chronic kidney disease (CKD) is linked to vascular calcification, increasing mortality.
Klotho-hypomorphic (kl/kl) mice exhibit vascular calcification, hyperphosphataemia, and hyperaldosteronism, mirroring CKD complications.
Mineralocorticoids play a role in vascular osteoinductive signaling, exacerbating calcification.

Purpose of the Study:

To investigate the role of aldosterone in promoting vascular calcification in kl/kl mice and human aortic vascular smooth muscle cells (HAoSMCs).
To evaluate the therapeutic potential of spironolactone in reversing aldosterone-induced vascular calcification.

Main Methods:

Treatment of kl/kl mice and HAoSMCs with aldosterone and spironolactone.
Analysis of gene and protein expression related to osteogenic pathways (Pit1, Tnfα, Msx2, Cbfa1/Runx2, Osterix, Alp).
Silencing of the phosphate transporter Pit1 in HAoSMCs.

Main Results:

Spironolactone treatment reduced vascular osteoinductive processes and reversed osteogenic gene expression in kl/kl mice.
Aldosterone alone induced an osteogenic program in HAoSMCs, potentiated by phosphate.
Spironolactone and Pit1 silencing reversed aldosterone-induced osteogenic signaling in HAoSMCs.

Conclusions:

Vascular calcification in CKD is driven by both high phosphate and aldosterone-mediated osteoinductive signaling.
Spironolactone demonstrates potential in mitigating aldosterone's contribution to vascular calcification.
Further clinical studies are needed to confirm aldosterone's role and spironolactone's efficacy in CKD patients.