February 1, 2002Journal of Clinical Investigation

Fas receptor signaling inhibits glycogen synthase kinase 3β and induces cardiac hypertrophy following pressure overload

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Population

Cultured cardiomyocytes and lpr mice lacking a functional Fas receptor

Design

Preclinical

Authors

CBCornel BadorffGoethe University Frankfurt HRHartmut RuettenBoehringer Ingelheim (Germany)SMSven C. MuellerGhent University Hospital

Discussion

Member takes

Implication

Fas signaling may support compensatory hypertrophy in pressure overload; hypothesis-generating in mice and requires human validation before clinical consideration.

Structured PICO

Population

Cultured cardiomyocytes (in vitro) and lpr (lymphoproliferative disease) mice lacking a functional Fas receptor (in vivo)

Intervention

Fas ligand stimulation (in vitro) and pressure overload induction (in vivo)

Outcome

Cardiac hypertrophy, left ventricular dilatation, heart failure, and mortalitysurrogate

Fas receptor signaling is a novel pathway mediating cardiomyocyte hypertrophy and is required for compensation of pressure overload in vivo via inhibition of GSK3β.

Cite This Study

Badorff et al. (2002) studied this question.

synapsesocial.com/papers/6a7db08029cd345315cda30d https://doi.org/10.1172/jci200213779

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Implication

Fas signaling may support compensatory hypertrophy in pressure overload; hypothesis-generating in mice and requires human validation before clinical consideration.

Fas receptor signaling inhibits glycogen synthase kinase 3β and induces cardiac hypertrophy following pressure overload

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Fas receptor signaling inhibits glycogen synthase kinase 3β and induces cardiac hypertrophy following pressure overload

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider