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Updated: Aug 13, 2025
05:47
Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
Published on: May 10, 2021
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Myeloid CCN3 protects against aortic valve calcification
Peinan Tu1,2, Qian Xu1,3, Xianming Zhou1,4
1Cardiology Division, Emory University School of Medicine, 101 Woodruff Circle, Room 3004, Atlanta, GA, 30322, USA.
Cell Communication and Signaling : CCS
|January 20, 2023
Summary
Cellular communication network factor 3 (CCN3) deficiency in myeloid cells exacerbates aortic valve calcification by increasing BMP2. Macrophage-derived CCN3 plays a protective role against calcific aortic valve disease progression.
Area of Science:
- Cardiovascular Biology
- Cellular Signaling
- Immunology
Background:
- Cellular communication network factor 3 (CCN3) is known to regulate osteoblast differentiation.
- The role of CCN3 in valvular calcification and the mechanisms of macrophage involvement remain unclear.
- This study investigates the function of macrophage-derived CCN3 in calcific aortic valve disease (CAVD).
Discussion:
- Myeloid-specific CCN3 knockout mice exhibited impaired aortic valve function and increased calcification.
- CCN3 deficiency in macrophages led to increased production and secretion of bone morphogenic protein 2 (BMP2).
- Macrophage-derived CCN3 may exert anti-calcification effects by modulating BMP2 signaling in CAVD.
Key Insights:
- Myeloid CCN3 plays a critical role in regulating aortic valve calcification.
- CCN3 deficiency in macrophages enhances BMP2 production, promoting valvular calcification.
- Macrophage-derived CCN3 acts as a novel regulator in the pathogenesis of CAVD.
Outlook:
- Targeting myeloid CCN3 or BMP2 could offer therapeutic strategies for CAVD.
- Further research is needed to elucidate the precise molecular pathways linking CCN3, BMP2, and valvular interstitial cells.
- Investigating the upstream regulators of CCN3 in macrophages may reveal new therapeutic targets.
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