Calcific Aortic Valvular Disease (CAVD) is the most common valvular heart disease in western countries, and of adults >65y, approximately 25% have aortic sclerosis, which is the pathological precursor to aortic stenosis (AS). The pathogenic mechanism of CAVD is strongly linked with the anatomical structure and location. Valvular interstitial cells account for the majority of the overall cell population in AV tissue, most of which representing quiescent fibroblast-like cells. The osteogenic differentiation of VICs is the core mechanism of the progression of CAVD, and followed by collagen deposition, ECM remodeling, leads to the VIC-mediated bone formation eventually. Valvular endothelial cells form the physical barrier in the surface of the AV, sensing environmental changes including mechanical stress and circulating cytokines. The rupture of VECs will abet the infiltration of lipids and immune cells which would further activate VICs. Despite that numerous promising therapeutic targets have been found in other cardiovascular diseases, none of them have been proven to be effective in reversing the process of CAVD, which reveals the importance of comprehensively lucubrate into the pathogenic mechanism of this disease. At the same time, the inevitable decay of bioprosthetic valve remains a vexing problem.
In this research topic, we would like to investigate novel biomolecular mechanism in the progression of aortic valve calcification, which would provide a new perspective for clinical drug research and development. We would recommend the discovery of pathogenic mechanism form the standpoint of disease spectrum which ranges from microscopic changes to fibro-calcific leaflet remodeling. We also want to shed some light on the treatment of CAVD where existing pharmaceutical consistently fails to impact its progression. Every step of your research will advance treatment of CAVD.
We welcome submissions on the following topics, but are not limited to:
- The interaction of different types of valvular cells in the process of valvular calcification
- Establishment of in vitro model to study the interaction of each cell type
- The importance of Endo-MT in the process of valvular calcification
- New biomolecular mechanism which regulates osteogenic differentiation of VICs
- Discovery of circulating biomarkers indicating the progression of CAVD
- Establishment of effective drug delivery system appropriate for the aortic valve
- Explore the decay causes of existing valve biomaterials
- Advanced pre-treatment of bioprosthetic valve to extend its period of validity
- Develop new valve material and show its advantages
Calcific Aortic Valvular Disease (CAVD) is the most common valvular heart disease in western countries, and of adults >65y, approximately 25% have aortic sclerosis, which is the pathological precursor to aortic stenosis (AS). The pathogenic mechanism of CAVD is strongly linked with the anatomical structure and location. Valvular interstitial cells account for the majority of the overall cell population in AV tissue, most of which representing quiescent fibroblast-like cells. The osteogenic differentiation of VICs is the core mechanism of the progression of CAVD, and followed by collagen deposition, ECM remodeling, leads to the VIC-mediated bone formation eventually. Valvular endothelial cells form the physical barrier in the surface of the AV, sensing environmental changes including mechanical stress and circulating cytokines. The rupture of VECs will abet the infiltration of lipids and immune cells which would further activate VICs. Despite that numerous promising therapeutic targets have been found in other cardiovascular diseases, none of them have been proven to be effective in reversing the process of CAVD, which reveals the importance of comprehensively lucubrate into the pathogenic mechanism of this disease. At the same time, the inevitable decay of bioprosthetic valve remains a vexing problem.
In this research topic, we would like to investigate novel biomolecular mechanism in the progression of aortic valve calcification, which would provide a new perspective for clinical drug research and development. We would recommend the discovery of pathogenic mechanism form the standpoint of disease spectrum which ranges from microscopic changes to fibro-calcific leaflet remodeling. We also want to shed some light on the treatment of CAVD where existing pharmaceutical consistently fails to impact its progression. Every step of your research will advance treatment of CAVD.
We welcome submissions on the following topics, but are not limited to:
- The interaction of different types of valvular cells in the process of valvular calcification
- Establishment of in vitro model to study the interaction of each cell type
- The importance of Endo-MT in the process of valvular calcification
- New biomolecular mechanism which regulates osteogenic differentiation of VICs
- Discovery of circulating biomarkers indicating the progression of CAVD
- Establishment of effective drug delivery system appropriate for the aortic valve
- Explore the decay causes of existing valve biomaterials
- Advanced pre-treatment of bioprosthetic valve to extend its period of validity
- Develop new valve material and show its advantages
