FIG. 5.

Potential mechanisms by which TXNIP can affect cellular redox state. Visual representation of our current knowledge regarding the potential ways in which TXNIP affects cellular redox state. TXNIP and glucose form an auto-feedback loop together, regulating each other. Glucose is needed to produce NADPH such as via the pentose phosphate pathway. Too much glucose can lead to increased ROS production by the mitochondria in two ways: (1) Increased metabolic flux through mitochondria increases ROS production; (2) excess glucose rigidifies mitochondrial membranes, leading to less efficient OXOPHOS flux and increased ROS. NADPH is consumed by intrinsic cellular defense mechanisms to counter ROS. NADPH is also consumed when oxidized Txn is regenerated. ROS, reactive oxygen species; Txn, thioredoxin.