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Fig 1. Schematic diagram of mechanisms and cellular events involved in organ fibrosis. After suffering sustaining and diverse stimuli including drugs, mechanical damage, inflammation, and infection, complicated cellular signaling transduction related with fibrosis will happen in several organs. Multiple cell types including quiescent hepatic stellate cells, pancreatic stellate cells are activated into myofibroblasts, and outcomes to the excessive deposition of ECM, reflecting the early formation of fibrosis.
Fig 2. Difference between apoptosis and necroptosis. Apoptosis is a caspase-dependent RCD which characterized by cell membrane blistering, cell contraction, nuclear fracturing, chromosome concentration and chromosomal DNA fragmentation. Different from apoptosis, necroptosis is a type caspase-independent RCD form which characterized by increased cell membrane permeability, plasmalemma ruptures, general swelling of cytoplasm and organelles, and overflow of cell components into the microenvironment.
Fig 3. The detailed diagram of Necroptosis Signal pathway. When caspase-8 is inhibited, the active RIPK1 will interact with RIPK3 to cause its phosphorylation and forming a necrosome complex. Phosphorylated RIPK3 activate MLKL to form a homotrimer by its amino-terminal coiled-coil domain, further mediate transient receptor potential melastatin related 7 induce Ca(2+) influx and locates to the cell plasmalemma to destroy the integrity of the plasmalemma by forming micro pores. Zα domains of ZBP1 can sense endogenous Z-form nucleic acids to activite RIPK3-dependent necroptosis .
Fig 4. Necroptosis related signal pathway. Necroptosis signal pathway is closely related with several other forms of RCD containing apoptosis, autophagy and ferroptosis. Casepase 8 is a key switch between apoptosis and necroptosis, due to its cleaving capacity of RIPK1 and RIPK3. Autophagy-related protein 16-1 can interdicts necroptosis. As the primary endogenous inhibitor of ferroptosis, glutathione peroxidase 4 can mediates powerful necroptosis inhibition effects. Besides different forms of RCD mentioned above, necroptosis also intimately connected with inflammation, oxidative stress and many other physiopathological processes.
Table 1. The small molecular inhibitor of necroptosis