Vascular biology and bone formation: hints from HIF.
In this issue of the JCI, Wang, Clemens, and colleagues demonstrate that hypoxia-inducible factor alpha (HIF alpha) signaling in bone-building osteoblasts is central to the coupling of angiogenesis and long bone development in mice (see the related article beginning on page 1616). They show that bone formation controlled by osteoblast HIF alpha signaling is not cell autonomous but is coupled to skeletal angiogenesis dependent upon VEGF signaling. Thus, strategies that promote HIF alpha signaling in osteoblasts may augment bone formation and accelerate fracture repair.
Towler
Dwight A
DA
Department of Medicine, Center for Cardiovascular Research, Division of Bone and Mineral Diseases, Washington University School of Medicine, St. Louis, Missouri 63110, USA. dtowler@im.wustl.edu
D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins / Q000502:physiology*; D001846:Bone Development / Q000502:physiology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000502:physiology*; D051379:Mice; D008954:Models, Biological; D018919:Neovascularization, Physiologic; D010006:Osteoblasts / Q000502:physiology; D015398:Signal Transduction; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology; D000099162:Endothelial PAS Domain-Containing Protein 1
D051792:Basic Helix-Loop-Helix Proteins; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D042461:Vascular Endothelial Growth Factor A; D000099162:Endothelial PAS Domain-Containing Protein 1; C497443:Hif1a protein, mouse; C467480:vascular endothelial growth factor A, mouse