Figure 7.

Schematic diagram depicting proposed BI1-PHB2 signaling modality in AKI. In physiological settings (as shown in the right panel), BI1 interacts with and therefore promotes PHB2 retention into mitochondria with the assistance of the mitochondrial transport protein TIM23, preserving mitochondrial homeostasis and tubular viability. Pathological stress such as IRI (as shown on the left panel) suffers from loss of BI1, leading to poor MOM localization and translocation of PHB2 into MIM. As a result, PHB2 is lost into cytoplasm (loss of mitochondrial retention) to trigger mitochondrial damage.