Figure 10.

Cell death through lysosome membrane disruption and UPR pathway activation. (a) Damage caused by the oxidative stress due to photodynamic therapy in the lysosome membrane releases the cathepsins D and B into the cytoplasm. Cathepsins D and B cleave Bid into tBid, which increases the permeability of the mitochondria membrane. Change in the permeability induces mitochondria-dependent apoptosis. (b) Oxidative stress caused due to photodynamic therapy increases misfolding of the proteins in the endoplasmic reticulum. When the misfolding surpasses the threshold, it triggers unfolded protein response (UPR). UPR activates the IRE1a receptor that binds with procaspase-12 to cleave procaspase-12 to caspase-12. Caspase-12 induces the cleavage of caspase-9 and caspase-3, which leads to mitochondria-dependent apoptosis.