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Shear-Sensitive Genes in Aortic Valve Endothelium
Joan Fernández Esmerats1, Jack Heath1, Hanjoong Jo1
1Department of Biomedical Engineering, Emory University and Georgia Institute of Technology , Atlanta, Georgia .
Antioxidants & Redox Signaling
|December 10, 2015
Summary
Calcific aortic valve disease (CAVD) mechanisms are unclear, hindering non-surgical treatments. Understanding valve endothelium mechanosensing and signaling pathways is crucial for developing future therapies to avoid surgery.
Area of Science:
- Cardiovascular Biology
- Mechanobiology
- Endothelial Cell Signaling
Background:
- Calcific aortic valve disease (CAVD) lacks effective non-surgical treatments due to poorly understood underlying mechanisms.
- The aortic valve endothelium normally adapts to hemodynamic forces, but this adaptation is impaired in CAVD, leading to dysfunction and inflammation.
Purpose of the Study:
- To review the role of mechanical forces, mechanosensors, and signaling pathways in the aortic valve endothelium in the context of CAVD.
- To highlight the current understanding of how mechanical stimuli influence cellular phenotype and contribute to CAVD pathogenesis.
Main Methods:
- Review of existing literature on valvular structure, mechanobiology, and endothelial cell signaling in CAVD.
- Exploration of key signaling pathways including TGF-β, Wnt/β-catenin, NADPH oxidase, and microRNA regulation.
Main Results:
- Mechanical forces are sensed by endothelial mechanosensors, triggering downstream signaling cascades.
- Mechanosensitive genes are upregulated, altering cellular phenotype and promoting inflammation and CAVD.
- NADPH oxidase, reactive oxygen species/nitrogen species, and microRNAs play significant roles in the cellular response to mechanical stimuli.
Conclusions:
- A deeper understanding of aortic valve endothelium mechanobiology is essential for developing novel therapeutic strategies for CAVD.
- Future research focusing on these mechanisms could lead to treatments that prevent or reverse valve calcification, avoiding surgical intervention.
