What is the clinical evidence from this study?

Study design: Other. Population: Calcific aortic valve disease. Intervention: Cadherin-11 (CDH11) deletion vs. Wild-type (Cdh11+/+). Primary outcome: Mechanobiological behavior of valvular interstitial cells (contractility and focal adhesions).

October 25, 2018AJP Heart and Circulatory PhysiologyOpen Access

Cadherin-11 as a regulator of valve myofibroblast mechanobiology

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Key result

Cadherin-11 influences valvular interstitial cell contractility by regulating focal adhesions and inflammatory cytokine secretion, mediating the myofibroblast disease phenotype.

Population

Aortic valve interstitial cells harvested from Cdh11+/+, Cdh11+/−, and Cdh11−/− immortomice, and aortic…

Comparison

CDH11 deletion and exposure to inflammatory… vs Wild-type (Cdh11+/+) cells and mice

Design

Preclinical

Authors

MBMeghan BowlerNova Southeastern University MBMatthew R. BersiWashington University in St. Louis LRLarisa RyzhovaMaineHealth

Discussion

Member takes

Implication

May position CDH11 as target in calcific aortic valve disease; leaves open whether modulation alters progression in vivo.

Structured PICO

Population

Aortic valve interstitial cells harvested from Cdh11+/+, Cdh11+/−, and Cdh11−/− immortomice, and aortic valves from Cdh11+/+, Cdh11+/−, and Cdh11−/− mice

Exposure

CDH11 deletion and exposure to inflammatory cytokines (TGF-β1 and IL-6)

Comparator

Wild-type (Cdh11+/+) cells and mice

Outcome

Mechanobiological behavior, contractility, and myofibroblast phenotypesurrogate

Cadherin-11 is a key mediator of the myofibroblast phenotype in valvular interstitial cells, suggesting it could be a multifaceted therapeutic target for calcific aortic valve disease.

Cite This Study

Bowler et al. (2018) studied Calcific aortic valve disease. Cadherin-11 (CDH11) deletion vs. Wild-type (Cdh11+/+) was evaluated on Mechanobiological behavior of valvular interstitial cells (contractility and focal adhesions). Cadherin-11 influences valvular interstitial cell contractility by regulating focal adhesions and inflammatory cytokine secretion, mediating the myofibroblast disease phenotype.

synapsesocial.com/papers/6a9a1bb1352e687f024d4073 https://doi.org/10.1152/ajpheart.00277.2018

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October 25, 2018AJP Heart and Circulatory PhysiologyOpen Access

Cadherin-11 as a regulator of valve myofibroblast mechanobiology

View Full Paper

Ask AI

Bookmark

Key result

Cadherin-11 influences valvular interstitial cell contractility by regulating focal adhesions and inflammatory cytokine secretion, mediating the myofibroblast disease phenotype.

Population

Aortic valve interstitial cells harvested from Cdh11+/+, Cdh11+/−, and Cdh11−/− immortomice, and aortic…

Comparison

CDH11 deletion and exposure to inflammatory… vs Wild-type (Cdh11+/+) cells and mice

Design

Preclinical

Authors

MBMeghan BowlerNova Southeastern University MBMatthew R. BersiWashington University in St. Louis LRLarisa RyzhovaMaineHealth

Discussion

Member takes

Implication

May position CDH11 as target in calcific aortic valve disease; leaves open whether modulation alters progression in vivo.

Structured PICO

Population

Aortic valve interstitial cells harvested from Cdh11+/+, Cdh11+/−, and Cdh11−/− immortomice, and aortic valves from Cdh11+/+, Cdh11+/−, and Cdh11−/− mice

Exposure

CDH11 deletion and exposure to inflammatory cytokines (TGF-β1 and IL-6)

Comparator

Wild-type (Cdh11+/+) cells and mice

Outcome

Mechanobiological behavior, contractility, and myofibroblast phenotypesurrogate

Cadherin-11 is a key mediator of the myofibroblast phenotype in valvular interstitial cells, suggesting it could be a multifaceted therapeutic target for calcific aortic valve disease.

Cite This Study

synapsesocial.com/papers/6a9a1bb1352e687f024d4073 https://doi.org/10.1152/ajpheart.00277.2018

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