To Breathe or Not to Breathe: The Role of Oxygen in Bone Marrow-Derived Mesenchymal Stromal Cell Senescence

Figure 1

Schematic overview of the effects of hypoxia on BMSC senescence. Oxygen depletion induces or activates a number of cellular processes that delay or reverse cellular senescence in BMSCs. These include induction of stem cell-specific genes, upregulation of the HIF pathway and its effectors, or activation of autophagy. Parallel, hypoxia represses prosenescence factors like production of reactive oxygen species or expression of genes involved in cell cycle arrest and reduce activity of signaling cascades like the mTOR pathway. Abbreviations used are OCT4: octamer-binding protein 4; FABP3: fatty acid binding protein 3; TWIST: basic helix-loop-helix transcription factor; HIF1: hypoxia-inducible factor 1; IHH: Indian Hedgehog protein; MIF: macrophage inhibitory factor; SATB2: special AT-rich binding protein 2; mTOR: mammalian target of rapamycin; ROS: reactive oxygen species.