Skip to main content
Fig. 2 | Journal of Translational Medicine

Fig. 2

From: Inflammatory signaling in NASH driven by hepatocyte mitochondrial dysfunctions

Fig. 2

Liver inflammatory processes under conditions of oxidative stress in impaired mitochondria. Mitochondrial dysfunction triggers ROS production in OXPHOS. The damaged mtDNA formed under stress conditions is released into the cytosol, triggering certain inflammatory processes. NRLP3 inflammasome activation, TLR9 signaling, and activation of the cGAS-STING pathway generate inflammatory mediators, such as cytokines, including interferons, or IFNs. OXPHOS oxidative phosphorylation, OGG1 8-oxoguanine DNA glycosylase-1, FEN1 Flap Structure-Specific Endonuclease 1, VDAC voltage-dependent anion channel, IMM and OMM inner and outer mitochondrial membrane, respectively, NRLP3 NLR Family Pyrin Domain Containing 3, IL interleukin, Cas-1 caspase 1, TLR9 toll-like receptor 9, MyD88 myeloid differentiation primary response 88, cGAS cyclic GMP–AMP synthase, cGAMP cyclic guanosine monophosphate–adenosine, STING stimulator of interferon genes, IRF3 interferon regulatory factor 3. Figure created with BioRender (http://www.BioRender.com)

Back to article page