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Mechanisms of aortic stenosis
Hirokuni Akahori1, Takeshi Tsujino2, Tohru Masuyama1
1Division of Cardiovascular Medicine and Coronary Artery Disease, Hyogo College of Medicine, Nishinomiya, Japan.
Journal of Cardiology
|December 21, 2017
Summary
Degenerative aortic valve stenosis involves complex processes like fibrosis and inflammation. Nuclear factor-kappa B (NF-κB) and bone morphogenetic protein 2 (BMP2) signaling pathways are key drivers of valve calcification and angiogenesis.
Area of Science:
- Cardiovascular Biology
- Pathobiology
- Molecular Medicine
Background:
- Degenerative aortic valve stenosis (AS) is a complex disease.
- Key pathological features include fibrosis, inflammation, oxidative stress, angiogenesis, hemorrhage, and osteogenic differentiation.
Purpose of the Study:
- To summarize the mechanisms of valve calcification and angiogenesis in AS.
- To highlight nuclear factor-kappa B (NF-κB) as a therapeutic target.
Main Methods:
- Literature review and pathway analysis.
- Focus on signaling cascades involving NF-κB, bone morphogenetic protein 2 (BMP2), and hypoxia-inducible factor-2 (HIF-2).
Main Results:
- NF-κB activates BMP2 via interleukin-6, promoting osteogenic differentiation through Wnt signaling and Runx2/Cbfa1.
- NF-κB signaling also influences the hypoxia-inducible factor-2 axis, contributing to calcification and angiogenesis.
- Angiogenesis and associated hemorrhage are implicated in AS progression, despite the valve's avascular nature.
Conclusions:
- The NF-κB and BMP2 signaling pathways are central to the pathogenesis of degenerative AS.
- Targeting NF-κB may offer a therapeutic strategy to inhibit valve calcification and angiogenesis.
- Further research is needed to understand the role of angiogenesis in this disease.
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