Table 1.
Disease model | Probable necroptosis inducer | Downstream signaling | Nec-1 effects | Ref. |
Ethanol induced liver injury | TNF-α | JNK acts downstream of RIP3 | No effect | [16] |
Ethanol induced liver injury | TNF-α | No information | No information | [31] |
APAP-induced liver toxicity | Unknown | JNK acts downstream of RIP3 | Protective | [17] |
APAP-induced liver toxicity | Unknown | No information | Protective | [32] |
APAP-induced liver toxicity | Unknown | JNK acts downstream of RIP1 | Protective | [15] |
Con-A induced hepatitis model | TRAIL | PARP-1 acts downstream of RIP3 | Protective | [33] |
Con-A-induced hepatitis | Unknown | No information | Protective | [34] |
Liver sepsis model | FasL | No information | Hepatotoxic | [25] |
APAP: Acetaminophen; Con-A: Concanavalin; TNF-α: Tumor necrosis factor-α; JNK: C-Jun N-terminal kinase; RIP3: Receptor-interacting serine-threonine kinase 3; TRAIL: TNF-related apoptosis-inducing ligand; Nec: Necrostatin.