Figure 4.

Interplay between SIRT1, HIF1a and ROS during HBOT. Under normoxia, PHD senses oxygen and leads to the degradation of HIF1a. Hypoxia inhibits PHD, leading to an increase in HIF1a, while intermittent HBOT elevates antioxidants, which leads to inhibition of PHD, therefore mimicking a hypoxic state and also activating HIF1a. In a parallel by interwind pathway, hypoxia causes inhibition of SIRT1 via changes in NADH/NAD⁺ ratio that can lead to inhibition of mitochondrial biogenesis, while intermittent HBOT activates SIRT1, leading to an activation of mitochondrial biogenesis.