ArticleHepatology (Baltimore, Md.)2020
miR-210 Participates in Hepatic Ischemia Reperfusion Injury by Forming a Negative Feedback Loop With SMAD4.
Article in Hepatology (Baltimore, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- MicroRNAs in Tumor Endothelial Cells: Regulation, Function and Therapeutic Applications.Cells · 2023Pooled it
- TLR4 maintains Treg-mediated protection against adverse outcomes in a model of hepatic surgical stress.The Journal of clinical investigation · 2026Article
- miRNA-Mediated Regulation of γ-Globin to β-Globin Switching: Therapeutic Potential in β-Hemoglobinopathies.International journal of molecular sciences · 2026Review
- Exploring the Molecular Mechanisms of Autophagy-related Genes in Hepatic Ischemia/Reperfusion Injury Using Bioinformatics.Transplantation direct · 2025Article
- Current status and perspective on molecular targets and therapeutic intervention strategy in hepatic ischemia-reperfusion injury.Clinical and molecular hepatology · 2024Review
- The deubiquitinase OTUD1 stabilizes NRF2 to alleviate hepatic ischemia/reperfusion injury.Redox biology · 2024Article
- Bile acids attenuate hepatic inflammation during ischemia/reperfusion injury.JHEP reports : innovation in hepatology · 2024Article
- Pim-1 kinase protects the liver from ischemia reperfusion injury by regulating dynamics-related protein 1.iScience · 2024Article
- Targeting NF-κB in Hepatic Ischemia-Reperfusion Alleviation: from Signaling Networks to Therapeutic Targeting.Molecular neurobiology · 2024Review
- Lactobacillus reuteri mitigates hepatic ischemia/reperfusion injury by modulating gut microbiota and metabolism through the Nrf2/HO-1 signaling.Biology direct · 2024Article
- MiR-148b Caused Liver Injury in Rats with Traumatic Hemorrhagic Shock by Inhibiting SIRT6 Expression.Current molecular medicine · 2024Article
- VE-822 upregulates the deubiquitinase OTUD1 to stabilize FHL1 to inhibit the progression of lung adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Silencing lncRNA KCNQ1OT1 reduced hepatic ischemia reperfusion injury-induced pyroptosis by regulating miR-142a-3p/HMGB1 axis.Molecular and cellular biochemistry · 2023Article
- Hepatocyte SGK1 activated by hepatic ischemia-reperfusion promotes the recurrence of liver metastasis via IL-6/STAT3.Journal of translational medicine · 2023Article
- From cerebral ischemia towards myocardial, renal, and hepatic ischemia: Exosomal miRNAs as a general concept of intercellular communication in ischemia-reperfusion injury.Molecular therapy. Nucleic acids · 2022Review
- MicroRNAs: Novel Targets in Hepatic Ischemia-Reperfusion Injury.Biomedicines · 2022Review
- Development of a tRNA-derived small RNA diagnostic and prognostic signature in liver cancer.Genes & diseases · 2022Article
- Exosomal microRNA-618 derived from mesenchymal stem cells attenuate the progression of hepatic fibrosis by targeting Smad4.Bioengineered · 2022Article
- Article
- MicroRNAs in peripheral artery disease: potential biomarkers and pathophysiological mechanisms.Therapeutic advances in cardiovascular diseaseArticle
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsHepatic ischemia-reperfusion (IR) injury is a major complication of liver transplantation, resection, and hemorrhagic shock. Hypoxia is a key pathological event associated with IR injury. MicroRNA-210 (miR-210) has been characterized as a micromanager of hypoxia pathway. However, its function and mechanism in hepatic IR injury is unknown. APPROACH AND
resultsIn this study, we found miR-210 was induced in liver tissues from patients subjected to IR-related surgeries. In a murine model of hepatic IR, the level of miR-210 was increased in hepatocytes but not in nonparenchymal cells. miR-210 deficiency remarkably alleviated liver injury, cell inflammatory responses, and cell death in a mouse hepatic IR model. In vitro, inhibition of miR-210 decreased hypoxia/reoxygenation (HR)-induced cell apoptosis of primary hepatocytes and LO2 cells, whereas overexpression of miR-210 increased cells apoptosis during HR. Mechanistically, miR-210 directly suppressed mothers against decapentaplegic homolog 4 (SMAD4) expression under normoxia and hypoxia condition by directly binding to the 3' UTR of SMAD4. The pro-apoptotic effect of miR-210 was alleviated by SMAD4, whereas short hairpin SMAD4 abrogated the anti-apoptotic role of miR-210 inhibition in primary hepatocytes. Further studies demonstrated that hypoxia-induced SMAD4 transported into nucleus, in which SMAD4 directly bound to the promoter of miR-210 and transcriptionally induced miR-210, thus forming a negative feedback loop with miR-210.
conclusionsOur study implicates a crucial role of miR-210-SMAD4 interaction in hepatic IR-induced cell death and provides a promising therapeutic approach for liver IR injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.