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editorial
. 2016 Jul 30;7(32):50820–50821. doi: 10.18632/oncotarget.10970

Figure 1. Pathophysiological consequences of defective FA gene-mediated selective autophagy.

Figure 1

In a wild-type cells (left panels), viruses and damaged mitochondria are targeted by selective autophagy. This process removes pro-inflammatory pathogenassociated molecular patterns (PAMPs; e.g. viral nucleic acids) and danger associated molecular patterns (DAMPs; e.g. mitochondrial (mt) ROS). Defective clearance of selective autophagy substrates in FA gene-deficient cells (right panels) results in persistence of PAMPs and DAMPs, increased inflammasome activation, and oxidative genotoxic stress.