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. 2022 Jan 4;8:757336. doi: 10.3389/fmed.2021.757336

Table 2.

Summarization of IPC/IPostC in liver IRI.

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.