Table 2.
IPC or IPostC | Data origin | Main effects and conclusion | References |
---|---|---|---|
IPC | Rat model | IPC ameliorates liver IRI and restores mitochondrial function maybe via HO-1-mediated autophagy | (52) |
IPC | Mouse model | Combined IPC and rapamycin protects against hepatic IRI attributing to restored autophagy activation | (62) |
IPC | Rat model | Pretreatment with a slight of oxidative stress can trigger cellular adaptation protects by maintaining mitochondrial function. | (8) |
IPC | Mouse model | IPC alleviates liver IRI by decreasing TIM4 expression. | (63) |
IPC | Mouse model | RIPC diminishes hepatic IRI mediated by KATP through inhibition of HMGB1 induced TLR4/MyD88/NF-κB signaling pathway. | (64) |
IPC | Clinical trial | RIPC neither significantly improves liver transaminase level nor decreased the incidence of EAD and PNF. | (65) |
IPC | Clinical trial | RIPC does not improve liver function in living donor hepatectomy. | (66) |
IPostC | Rat model | IPostC protects against liver IRI possibly via the GSK-3ß/Fyn/Nrf2 pathway. | (67) |
IPostC | Rat model | IPostC protects against IRI mediated by microRNA-183 by repressing the expression of Apaf-1. | (68) |
IPostC | Mouse model | Mmu_circRNA_005186-miR-124-3p-Epha2 pathway may be the key axis for IPostC to attenuate hepatic IRI. | (69) |
IPostC | Clinical trial | Remote IPostC does not exhibit any improvements and clinical benefits preoperatively. | (70) |
IPostC | Clinical trial | IPostC does not influence postoperative AST peak values, however, a better tolerance to IRI are observed. | (71) |
HO-1, heme oxygenase-1; TIM4, T-cell immunoglobulin and mucin domain molecule-4; TLR4, Toll-like receptors; MyD88, myeloiddifferentiationfactor88; NF-κB, nuclear factor kappa B; EAD, early allograft dysfunction; PNF, primary graft non-function; GSK3β, glycogen synthase kinase-3; Nrf2, nuclear respiratory factor 2. Apaf-1, apoptotic protease activating factor-1.