Related Experiment Video
Updated: Oct 8, 2025

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
Published on: May 10, 2021
Emodin alleviates aortic valvular calcification by inhibiting the AKT/FOXO1 pathway
1Department of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Insights
Emodin effectively alleviates high-calcium-induced valvular calcification by suppressing AKT/FOXO1 signaling. This natural compound shows promise as a therapeutic strategy for treating valvular calcification in patients.
Area of Science:
- Biomedical research
- Pharmacology
- Cardiovascular disease
Background:
- Valvular calcification is a growing health concern, particularly in the elderly.
- Current treatments for valvular calcification are limited, highlighting the need for new therapeutic agents.
Purpose of the Study:
- To investigate the suppressive effects of emodin on high-calcium-induced valvular calcification.
- To elucidate the underlying molecular mechanisms of emodin's action.
Main Methods:
- Valvular calcification was induced in mice using vitamin D.
- Porcine aortic valve interstitial cells (PAVICs) were used to assess emodin's effects on cell viability, apoptosis, and osteogenic gene expression.
- The role of AKT/FOXO1 signaling was examined using specific activators and inhibitors.
Main Results:
- Emodin (5 μM) reduced calcium accumulation and osteogenic gene upregulation in PAVICs under high-calcium conditions.
- In vivo, emodin treatment decreased calcium content in serum, valves, and arteries of mice with induced valvular calcification.
- Emodin reversed the upregulation of p-AKT and p-FOXO1, key components of the AKT/FOXO1 signaling pathway.
Conclusions:
- Emodin demonstrates a significant therapeutic potential in alleviating valvular calcification.
- The mechanism involves the suppression of the AKT/FOXO1 signaling pathway.
- These findings offer novel insights for developing emodin-based treatments for clinical valvular calcification.
Background:
Valvular calcification commonly occurs in elderly individuals, and is increasingly considered an important economic and health burden. However, no efficient drugs against valvular calcification are available. The present work aimed to examine emodin's suppressive effect on high-calcium-dependent valve calcification and explore the underpinning mechanisms.
Methods:
Experiments were carried out in mice receiving vitamin D (Vit D) to induce valvular calcification.
Results:
Cell viability and apoptosis assays demonstrated celastrol suppressed proliferation and increased apoptosis in porcine aortic valve interstitial cells (PAVICs) at concentrations higher than 10 μM. Emodin (5 μM) attenuated the upregulation of osteogenic genes as well as calcium accumulation in PAVICs under high-calcium conditions. The elevations of calcium content in serum and valve, and calcium accumulation in valve and artery were suppressed by emodin in mice with valvular calcification after joint treatment with adenine and Vit D. In addition, p-AKT and p-FOXO1 were upregulated in PAVICs under high-calcium conditions, and this effect was reversed by emodin treatment. SC79, an AKT activator, reversed emodin's suppressive effects on increased calcium content, calcium deposition and osteogenic gene expression in PAVICs induced by calcific medium.
Conclusions:
These data demonstrated emodin alleviates high-calcium-associated valvular calcification via AKT/FOXO1 signaling suppression, providing new insights into therapeutic strategies for clinical valvular calcification.
More Related Videos
Related Concept Videos
Calmodulin-dependent Signaling
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
TGF - β Signaling Pathway
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antihypertensive Drugs: Action of Calcium Channel Blockers
Nitric Oxide Signaling Pathway
Aortic Regurgitation III: Medical Management

