Fig. 1.

Oxidative stress helps modulate HIF1α levels. In the cell depicted, when the mitochondrial respiratory chain functions appropriately, O₂ is consumed at COX, which keeps O₂ from accumulating and creates a HIF1α setpoint. With mitochondrial respiratory chain failure, intracellular hyperoxia can develop, with a consequent reduction in HIF1α. The respiratory chain dysfunction can cause electron egress from the mitochondria and subsequent production of free radicals and hydrogen peroxide, which can boost HIF1α levels by relieving hyperoxia or by accomplishing HIF1α stabilization. The thickness of the line leading from HIF1α to the nucleus is intended to confer greater versus lesser amounts of HIF1α signaling within the cell. Mito, mitochondria