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Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification
Published on: November 20, 2017
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Morusin Alleviates Aortic Valve Calcification by Inhibiting Valve Interstitial Cell Senescence Through
Zongtao Liu1, Kan Wang1, Chen Jiang1
1Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|March 19, 2024
Summary
Morusin, a natural compound, combats cellular senescence in aortic valve cells, offering a potential treatment for calcific aortic valve disease (CAVD). It activates anti-aging pathways, reducing oxidative stress and preventing valve calcification.
Area of Science:
- Cardiovascular Biology
- Cellular Aging
- Pharmacology
Background:
- Cellular senescence of aortic valve interstitial cells (VICs) drives calcific aortic valve disease (CAVD) progression.
- The exact mechanisms of VIC senescence are not fully understood, necessitating new therapeutic targets.
- Morusin exhibits known anti-aging properties.
Purpose of the Study:
- To investigate the therapeutic potential of morusin in mitigating CAVD.
- To elucidate the molecular mechanisms by which morusin affects VIC senescence and osteogenic differentiation.
Main Methods:
- In vitro cellular experiments on VICs treated with morusin.
- Analysis of senescence markers, osteogenic differentiation, and key protein expressions (CCND1, Keap1, Trim 25).
- In vivo studies using ApoE-/- mice fed a high-fat diet, treated with morusin.
Main Results:
- Morusin suppressed VIC senescence and shifted differentiation away from osteogenesis in vitro.
- Morusin activated the Nrf2-mediated anti-aging pathway by downregulating CCND1 and promoting Keap1 degradation via Trim 25.
- Activation of Nrf2 led to increased antioxidant gene expression, reduced reactive oxygen species, and inhibited VIC osteogenic differentiation.
- In vivo, morusin treatment attenuated aortic valve calcification in a mouse model of CAVD.
Conclusions:
- Morusin demonstrates significant anti-aging effects on VICs, inhibiting senescence and osteogenic differentiation.
- The Nrf2 pathway is a key mediator of morusin's protective effects against CAVD.
- Morusin holds promise as a novel therapeutic agent for treating calcific aortic valve disease.
