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

Journal of Clinical Investigation

Volumn 109, Issue 3, 2002, Pages 373-381

  Badorff, Cornel ^a   Ruetten, Hartmut ^b   Mueller, Sven ^a   Stahmer, Meike ^a   Gehring, Doris ^b   Jung, Frank ^a   Ihling, Christian ^c   Zeiher, Andreas M ^a   Dimmeler, Stefanie ^a  

^a GOETHE UNIVERSITY   (Germany)

^b SANOFI AVENTIS DEUTSCHLAND GMBH   (Germany)

^c UNIVERSITY OF FREIBURG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ANGIOTENSIN; CASPASE; FAS ANTIGEN; FAS LIGAND; GLYCOGEN SYNTHASE KINASE 3BETA;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL TYPE; CONGESTIVE HEART FAILURE; CONTROLLED STUDY; ENZYME ACTIVATION; ENZYME ACTIVITY; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; HEART FAILURE; HEART MUSCLE CELL; HEART VENTRICLE HYPERTROPHY; HEART VENTRICLE PRESSURE; HUMAN; HUMAN CELL; HYPERTENSION; IN VIVO STUDY; MORTALITY; MOUSE; NEWBORN; NONHUMAN; PRIORITY JOURNAL; RAT; SIGNAL TRANSDUCTION;

EID: 0036172127     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI13779     Document Type: Article

References (25)

1. Signaling pathways for cardiac hypertrophy and failure
2. New epidemiologic perspectives concerning mild-to-moderate heart failure
3. Apoptosis in myocytes in end-stage heart failure
4. Death by design: Programmed cell death in cardiovascular biology and disease
5. Loss of a gp130 cardiac muscle cell survival pathway is a critical event in the onset of heart failure during biomechanical stress
6. Apoptosis by death factor
7. Caspase activation is required for T cell proliferation
8. The cardiac Fas (APO-1/CD95) Receptor/Fas ligand system: Relation to diastolic wall stress in volume-overload hypertrophy in vivo and activation of the transcription factor AP-1 in cardiac myocytes
9. Stretch-induced programmed myocyte cell death
10. Expression of FAS adjacent to fibrotic foci in the failing human heart is not associated with increased apoptosis
11. Proinflammatory consequences of transgenic fas ligand expression in the heart
12. Enteroviral protease 2A cleaves dystrophin: Evidence of cytoskeletal disruption in an acquired cardiomyopathy
13. Suppression of apoptosis by nitric oxide via inhibition of ICE-like and CPP32-like proteases
14. Inhibition of nitric oxide synthase potentiates ischemia/reperfusion-induced myocardial apoptosis via a caspase-3 dependent pathway
15. Activation of nitric oxide synthase in endothelial cells via Akt-dependent phosphorylation
16. 2-terminal kinases
17. 11 in cardiomyocytes
18. Glycogen synthase kinase-3beta is a negative regulator of cardiomyocyte hypertrophy
19. Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B
20. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand
21. 2-terminal kinase activity in in vivo pressure overload
22. Cardiotrophin-1 activates a distinct form of cardiac muscle cell hypertrophy. Assembly of sarcomeric units in series via gp130/leukemia inhibitory factor receptor-dependent pathways
23. Apoptosis in rat cardiac myocytes induced with Fas ligand: Priming for Fas-mediated apoptosis with doxorubicin
24. Rapid transactivation of the VEGF receptor KDR/Flk-1 by the bradykinin B2 receptor contributes to eNOS activation in cardiac capillary endothelial cells
25. Cell-extracellular matrix interactions stimulate the AP-1 transcription factor in an integrin-linked kinase- and glycogen synthase kinase 3-dependent manner