“…In this scenario, it is intriguing that apoptotic- and inflammatory-related intracellular pathways operating in AMD, including TLR/RAGEs, PKC, NF-kB, JAK/STAT, AKT/mTOR, and C3 complement, while impinging on the autophagy machinery and standard proteasomes, engage an alternative cytokine-inducible proteasome isoform, the immunoproteasome [ 38 , 84 , 127 , 164 , 165 , 166 , 167 , 168 , 169 , 170 ]. Contrarily from the standard proteasome, which is ubiquitously expressed, the immunoproteasome operates constitutively in immune tissues and cells, while being induced by oxidative stress and inflammatory cytokines in other kinds of cells, including neurons and glia of the retina and CNS [ 164 ].…”