In this issue of the JCI, Wang, Clemens, and colleagues
demonstrate that hypoxia-inducible factor α (HIFα)
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
HIFα signaling is not cell autonomous but is coupled to skeletal
angiogenesis dependent upon VEGF signaling. Thus, strategies that promote
HIFα signaling in osteoblasts may augment bone formation and
accelerate fracture repair.
