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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