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. 2019 Oct 25;20(21):5314. doi: 10.3390/ijms20215314

Figure 2.

Figure 2

Schematic representation of the mechanism of HMGB1 release and its pathological impact in the autophagy-deficient liver. Autophagy deficiency causes accumulation of p62, which can physically associate with KEAP1 to activate the antioxidative transcription factor, NRF2. Activation of NRF2 causes HMGB1 release via CASPASE 1/11-mediated inflammasomes. Extracellular HMGB1, via receptor for advanced glycation end products (RAGE), promotes ductular reaction and tumor development without affecting liver inflammation and fibrosis. Dotted lines indicate possible but unproven processes.