The mammalian FoxO (forkhead box O) transcription factors FoxO1, FoxO3 and FoxO4 represent one of several effector arms of the PI3K (phosphoinositide 3-kinase)–Akt signalling network that has been linked to cancer, metabolism and aging. Specific roles of the FoxOs in the vascular cell types have been investigated to reveal that they play redundant yet critical roles in the proliferation and survival of ECs (endothelial cells). Somatic deletions of all FoxOs engendered progressive, widespread and highly penetrant haemangiomas associated with altered proliferative/survival dynamics of ECs in our genetic model. Related work by Akt–FoxO manipulation reported differentially regulated genes in ECs that may represent novel FoxO targets, controlling EC growth and morphogenesis and mediating many of the consequences of FoxO inactivation in the endothelium. Further studies on the action of these surrogate genes may provide important new insights into how the PI3K–Akt–FoxO pathway could be exploited clinically to treat vascular diseases and lead to the invention of novel therapeutic approaches. Here recent studies elucidating the role of FoxOs in the maintenance of vascular homoeostasis and supporting that the mammalian FoxO family serves essential roles in the maintenance of vascular stability and the suppression of aberrant vascular outgrowth are discussed.
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October 2006
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Conference Article|
October 25 2006
FOXOs in the maintenance of vascular homoeostasis
J.-H. Paik
J.-H. Paik
1
*Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, U.S.A.
†Departments of Medicine and Genetics, Harvard Medical School, Boston, MA 02115, U.S.A.
1email Jihye_Paik@dfci.harvard.edu
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Publisher: Portland Press Ltd
Received:
June 27 2006
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2006 The Biochemical Society
2006
Biochem Soc Trans (2006) 34 (5): 731–734.
Article history
Received:
June 27 2006
Citation
J.-H. Paik; FOXOs in the maintenance of vascular homoeostasis. Biochem Soc Trans 1 October 2006; 34 (5): 731–734. doi: https://doi.org/10.1042/BST0340731
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