Liver ischemia/reperfusion injury (LIRI) is a common complication of liver surgery, and affects liver function post‑transplantation. However, the precise mechanism underlying LIRI has not yet been completely elucidated. Previous studies have demonstrated the involvement of a number of microRNAs (miRNAs/miRs) in liver pathophysiology. The objective of the present study was to determine the potential function and mechanism of miR‑101‑mediated regulation of autophagy in LIRI. Compared with the sham‑treated group, a significant decrease in miR‑101 and mechanistic target of rapamycin (mTOR) expression levels following ischemia/reperfusion (IR) were observed, along with an increased number of autophagosomes (P<0.001). The exogenous overexpression of miR‑101 has been demonstrated to inhibit autophagy during the LIRI response and the levels of mTOR and phosphorylated (p)‑mTOR expression are correspondingly elevated. However, compared with the miR‑NC group, miR‑101 silencing was associated with reduced mTOR and p‑mTOR levels and increased autophagy, as indicated by the gradual increase in the levels of the microtubule‑associated protein 1 light II (LC3II). The peak levels of LC3II were observed 12 h subsequent to reperfusion, which coincided with the lowest levels of miR‑101. In addition, inhibition of autophagy by 3‑methyladenine significant enhanced the protective effect of miR‑101 against LIRI, compared with the IR group (P<0.001). Altogether, miR‑101 attenuates LIRI by inhibiting autophagy via activating the mTOR pathway.

Interferon regulatory factor 1 (IRF-1) is a member of the IRF family. It is the first transcription factor to be identified that could bind to the interfer

Owing to oversights during the production process, a pair of errors were introduced into the above article. First, in the Materials and methods section, Animals and cell lines subsection, on p. 1332, line 12, the sentence starting here should have read as: 'The non‑tumorigenic mouse hepatocyte alpha mouse liver 12 (AML12) cell line was purchased from the Shanghai Cell Bank of Chinese Academy of Sciences (Shanghai, China)' (i.e., the abbreviation AML12 was expanded incorrectly). Secondly, the bottom row of data was accidentally omitted from Table I (pertaining to the Suzuki score for liver ischemia/reperfusion injury assessed to be severe).The fifth data row in the Table should have read, from left to right, as follows: Numerical assessment, '4'; Congestion, 'Severe (>60%)'; Vacuolization, 'Severe (>60%)'; and Necrosis, 'Severe (>60%)'.We regret that these errors were introduced into the published version of this paper, and apologize to the authors and the readership for the inconvenience caused. [the original article was published in International Journal of Molecular Medicine 43: 1331‑1342, 2019; DOI: 10.3892/ijmm.2019.4077].

Ischemia–reperfusion injury (IRI) represents a severe form of tissue or organ damage that occurs spontaneously and passively during the reperfusion process, following abrupt pathophysiological disturbances in the internal milieu. Alleviating and preventing IRI during organ resection or transplantation has long been a prevalent and intricate challenge in this field. Interferon regulatory factors (IRFs) constitute a superfamily of transcription factors that play pivotal roles in regulating diverse cellular biological functions, encompassing immune response modulation, inflammatory reaction control, cell proliferation and differentiation, and antiviral defense. The activation of IRFs and their downstream gene regulation primarily depend upon signal stimulation by three types of interferons (IFNs), forming an IFN-IRF-target gene cascade pathway. Consequently, the expression functions induced by IRFs under each IFN stimulus can exhibit markedly distinct characteristics. Recent studies have demonstrated that biological events involving IRFs are widespread across the cardiovascular system, central nervous system, and organs including the kidneys, liver, and intestine. Intervention targeting IRFs and their associated pathways has emerged as a significant research direction for preventing organ IRI. Nevertheless, the underlying regulatory mechanisms require further investigation and elucidation. This review aims to systematically expound the regulatory mechanisms and research advances concerning interferon regulatory factors (IRFs) and their related pathways in IRI across multiple systems and organs, from pathophysiological and molecular biological perspectives. This work not only illuminates the molecular basis of functional heterogeneity among IRFs but also proposes two innovative theoretical frameworks: the “dynamic regulatory network” and the “organ–IRF axis”. Future research ought to integrate single-cell sequencing, organoid models, and artificial intelligence prediction to elucidate the dynamic regulatory network of IRFs, thereby addressing the challenges of translational bottlenecks. Furthermore, the development of organ-specific delivery systems and heightened attention to the roles of IRFs in novel cell death mechanisms will furnish crucial support for translating research findings in this domain into clinical practice.

Background: Hepatic ischemia-reperfusion injury (HIRI) is an unavoidable event associated with liver relevant surgeries. Long-chain non-coding RNA, metastasis associated in lung denocarcinama transcript 1 (LncMALAT1) plays important role in tissue ischemia-reperfusion injury. The aim of the study is to characterize the mechanism of LncMALAT1 in the HIRI promotion. Methods: The constructed LncMALAT1 lentivirus was employed to stablish LncMALAT1 up- and down-regulating mice that were all subjected to 70% liver ischemia to create HIRI. The degree of liver tissue injury and hepatocyte apoptosis were visualized using hematoxylin-eosin staining, terminal dexynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate (dUTP) nick end labeling (TUNEL) method. LncMALAT1 expression was monitored using real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR). Western blot analysis was performed to evaluate autophagy and apoptosis-related proteins expression. Additionally, autophagosome rate was quantified employing transmission electronic microscopy (TEM). Finally, the confocal microscopy was used to observe specific mecherry-green fluorescent protein-microtubule-associated protein 1 light chain 3 (mcherry-GFP-LC3) in LncMALAT1 overexpressed/knockout cell under 1 hour hypoxia/12 hours re-oxygenation condition. The relative rescue experiment was performed using autophagy regulator of 3-methyladenine (3-MA)/rapamycin. The cell survival rate was detected by 3-(4,5-dimethylthiahiazol-2-yl)-2,5-diphenytetrazoliumromide (MTT) assay. Results: Compared to the sham-operated group, both the RNA expression of LncMALAT1 and liver damage were increased in all HIRI groups (p < 0.05). And 6 hours after reperfusion reached to the peak liver damage in line with the RNA expression of LncMALAT1. Upregulated LncMALAT1 in vivo and in vitro, TUNEL positive rate, autophagosome rate and mcherry-GFP-LC3 autophagy dots were significantly increased compared to the control group (p < 0.05). The protein expression of Caspase8, Cleaved-Caspase3, microtubule-associated protein 1 light chain 3 (LC3), autophagy related gene 12 (Atg12) were increased (p < 0.05), but the protein expression of sequestosome 1 (SQSTM1/p62), B cell lymphoma-2 (Bcl2), phosphorylated mechanistic target of rapamycin (p-mTOR) were decreased in LncMALAT1 upregulated group liken to the control group (p < 0.05). Nevertheless, downregulation of LncMALAT1 could alleviate the liver damage in vivo and in vitro. Importantly, the LncMALAT1 induced liver autophagy elevation that was responsible for severe apoptosis in HIRI, at least partially. Conclusions: LncMALAT1 enhanced liver autophagy leading to apoptosis aggravation and further hepatic ischemia-reperfusion injury in mice.