Abstract
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.