In vivo survival strategies for cellular adaptation to hypoxia: HIF1α-dependent suppression of mitochondrial oxygen consumption and decrease of intracellular hypoxia are critical for survival of hypoxic chondrocytes.

Hypoxia occurs not only in pathological conditions like cancer and ischemia and in a variety of physiological settings in the adult organism, but also during normal embryonic development. In the inner portion of the fetal growth plate, which is an avascular tissue originating from mesenchymal progenitor cells, chondrocytes experience physiological hypoxia. Hypoxia-Inducible Transcription Factor-1α (HIF1α), a crucial mediator of cellular adaptation to hypoxia, is an essential survival factor for fetal growth plate chondrocytes. This brief review summarizes our current understanding of the survival function of HIF1α during endochondral bone development. Published by Elsevier Inc.