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

Bone. 2020 Nov:140:115572. doi: 10.1016/j.bone.2020.115572. Epub 2020 Aug 5.

Abstract

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.

Keywords: Cell survival; Chondrocyte; Growth plate; HIF1α; Hypoxia; Mitochondrial respiration.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Bone Development
  • Cell Hypoxia
  • Chondrocytes*
  • Growth Plate*
  • Humans
  • Hypoxia
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Oxygen Consumption

Substances

  • Hypoxia-Inducible Factor 1, alpha Subunit