Figure 8.

Scheme depicting TSG101-mediated protection against endotoxin-induced cardiac dysfunction. TSG101 is bound to Parkin in the cytosol under basal conditions. However, upon endotoxin stress stimuli, Parkin is translocated to mitochondria with the help of TSG101, where it interacts with PINK1. This action allows binding of ubiquitin, recruitment of the autophagy adaptor LC3, and formation of autophagosomes around the damaged mitochondria. The mitochondria are then targeted to the lysosome for degradation.