Editorial on “Visualization of Human Aortic Valve Dynamics Using MRI With Sub‐Millisecond Temporal Resolution”

Author(s):  
Marshall S. Sussman
2003 ◽  
Vol 125 (6) ◽  
pp. 1412-1419 ◽  
Author(s):  
Michael Handke ◽  
Gudrun Heinrichs ◽  
Friedhelm Beyersdorf ◽  
Manfred Olschewski ◽  
Christoph Bode ◽  
...  

2014 ◽  
Vol 62 (S 01) ◽  
Author(s):  
C. Schmidtke ◽  
D. Richardt ◽  
A. Karluss ◽  
H.-H. Sievers

2021 ◽  
Vol 5 (sup1) ◽  
pp. 1-1
Author(s):  
Alex Khang ◽  
Chiara Camillo ◽  
Giovanni Ferrari ◽  
Michael S. Sacks

2020 ◽  
Vol 21 (23) ◽  
pp. 8917
Author(s):  
Francesco Vieceli Dalla Sega ◽  
Francesca Fortini ◽  
Paolo Cimaglia ◽  
Luisa Marracino ◽  
Elisabetta Tonet ◽  
...  

Calcific aortic valve disease (CAVD) is the result of maladaptive fibrocalcific processes leading to a progressive thickening and stiffening of aortic valve (AV) leaflets. CAVD is the most common cause of aortic stenosis (AS). At present, there is no effective pharmacotherapy in reducing CAVD progression; when CAVD becomes symptomatic it can only be treated with valve replacement. Inflammation has a key role in AV pathological remodeling; hence, anti-inflammatory therapy has been proposed as a strategy to prevent CAVD. Cyclooxygenase 2 (COX-2) is a key mediator of the inflammation and it is the target of widely used anti-inflammatory drugs. COX-2-inhibitor celecoxib was initially shown to reduce AV calcification in a murine model. However, in contrast to these findings, a recent retrospective clinical analysis found an association between AS and celecoxib use. In the present study, we investigated whether variations in COX-2 expression levels in human AVs may be linked to CAVD. We extracted total RNA from surgically explanted AVs from patients without CAVD or with CAVD. We found that COX-2 mRNA was higher in non-calcific AVs compared to calcific AVs (0.013 ± 0.002 vs. 0.006 ± 0.0004; p < 0.0001). Moreover, we isolated human aortic valve interstitial cells (AVICs) from AVs and found that COX-2 expression is decreased in AVICs from calcific valves compared to AVICs from non-calcific AVs. Furthermore, we observed that COX-2 inhibition with celecoxib induces AVICs trans-differentiation towards a myofibroblast phenotype, and increases the levels of TGF-β-induced apoptosis, both processes able to promote the formation of calcific nodules. We conclude that reduced COX-2 expression is a characteristic of human AVICs prone to calcification and that COX-2 inhibition may promote aortic valve calcification. Our findings support the notion that celecoxib may facilitate CAVD progression.


2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i247-i247
Author(s):  
Arseny Zabirnyk ◽  
Maria Bogdanova ◽  
Miguel D Ferrer ◽  
Maria Pérez ◽  
Mari-Liis Kaljusto ◽  
...  

2018 ◽  
Vol 96 (2) ◽  
pp. 208-214 ◽  
Author(s):  
Ateeque Siddique ◽  
Bin Yu ◽  
Kashif Khan ◽  
Ryan Buyting ◽  
Hamood Al-Kindi ◽  
...  

The cellular mechanisms that induce calcific aortic stenosis are yet to be unraveled. Wnt signaling is increasingly being considered as a major player in the disease process. However, the presence of Wnt Frizzled (Fzd) receptors and co-receptors LRP5 and 6 in normal and diseased human aortic valves remains to be elucidated. Immunohistochemistry and quantitative polymerase chain reaction were used to determine Fzd receptor expression in normal and calcified human aortic valve tissue, as well as human aortic valve interstitial cells (HAVICs) isolated from calcified and normal human aortic valves. There was significantly higher mRNA expression of 4 out of the 10 Fzd receptors in calcified aortic valve tissues and 8 out of the 10 in HAVICs, and both LRP5/6 co-receptors in calcified aortic valves (P < 0.05). These results were confirmed by immunohistochemistry, which revealed abundant increase in immunoreactivity for Fzd3, 7, and 8, mainly in areas of lipid core and calcified nodules of diseased aortic valves. The findings of abundant expression of Fzd and LRP5/6 receptors in diseased aortic valves suggests a potential role for both canonical and noncanonical Wnt signaling in the pathogenesis of human aortic valve calcification. Future investigations aimed at targeting these molecules may provide potential therapies for aortic valve stenosis.


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