ArticleTransplantation2015
Donor Hepatic Steatosis Induce Exacerbated Ischemia-Reperfusion Injury Through Activation of Innate Immune Response Molecular Pathways.
Article in Transplantation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Donor-Related Risk Factors for Normothermic Machine Perfusion in Liver Transplantation: A Meta-Analysis.Liver international : official journal of the International Association for the Study of the Liver · 2025Pooled it
- The Potentials of Stem Cell-Derived Exosomal MicroRNAs in Ferroptosis Modulation: Molecular Insights into Hepatoprotection, Neuroprotection, Cardioprotection, Renoprotection and Pulmonoprotection.Stem cell reviews and reports · 2026Review
- Epithelial membrane protein 1 drives hepatic stellate cell activation via the TLN1/FAK cascade in MASLD donor liver transplantation.Molecular biomedicine · 2025Article
- Molecular Mechanisms of Ischemia/Reperfusion Injury and Graft Dysfunction in Liver Transplantation: Insights from Multi-Omics Studies in Rodent Animal Models.International journal of biological sciences · 2025Review
- Programmed cell death, from liver Ischemia-Reperfusion injury perspective: An overview.Heliyon · 2024Review
- The role of ischaemia-reperfusion injury and liver regeneration in hepatic tumour recurrence.JHEP reports : innovation in hepatology · 2023Review
- Immune Features of Disparate Liver Transplant Outcomes in Female Hispanics With Nonalcoholic Steatohepatitis.Transplantation direct · 2023Article
- NO-IL-6/10-IL-1β axis: a new pathway in steatotic and non-steatotic liver grafts from brain-dead donor rats.Frontiers in immunology · 2023Article
- Liver Graft Proteomics Reveals Potential Incipient Mechanisms behind Early Renal Dysfunction after Liver Transplantation.International journal of molecular sciences · 2022Article
- The role of MLKL in Hepatic Ischemia-Reperfusion Injury of Alcoholic Steatotic Livers.International journal of biological sciences · 2022Article
- How useful is the machine perfusion in liver transplantation? An answer from a national survey.Frontiers in surgery · 2022Article
- miR-29a-3p in Exosomes from Heme Oxygenase-1 Modified Bone Marrow Mesenchymal Stem Cells Alleviates Steatotic Liver Ischemia-Reperfusion Injury in Rats by Suppressing Ferroptosis via Iron Responsive Element Binding Protein 2.Oxidative medicine and cellular longevity · 2022Article
- Clear mortality gap caused by graft macrosteatosis in Chinese patients after cadaveric liver transplantation.Hepatobiliary surgery and nutrition · 2020Article
- Involvement of kindlin-2 in irisin's protection against ischaemia reperfusion-induced liver injury in high-fat diet-fed mice.Journal of cellular and molecular medicine · 2020Article
- Therapeutics administered duringWorld journal of transplantation · 2020Review
- Metabonomic Profile of Macrosteatotic Allografts for Orthotopic Liver Transplantation in Patients With Initial Poor Function: Mechanistic Investigation and Prognostic Prediction.Frontiers in cell and developmental biology · 2020Article
- The Immunological Basis of Liver Allograft Rejection.Frontiers in immunology · 2020Review
- Receptor-Interacting Serine/Threonine-Protein Kinase 3 (RIPK3)-Mixed Lineage Kinase Domain-Like Protein (MLKL)-Mediated Necroptosis Contributes to Ischemia-Reperfusion Injury of Steatotic Livers.The American journal of pathology · 2019Article
- Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms.Liver international : official journal of the International Association for the Study of the Liver · 2019Review
- Complement Activation in Liver Transplantation: Role of Donor Macrosteatosis and Implications in Delayed Graft Function.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSevere liver steatosis is a known risk factor for increased ischemia-reperfusion injury (IRI) and poor outcomes after liver transplantation (LT). This study aimed to identify steatosis-related molecular mechanisms associated with IRI exacerbation after LT.
methodsPaired graft biopsies (n = 60) were collected before implantation (L1) and 90 minutes after reperfusion (L2). The LT recipients (n = 30) were classified by graft macrosteatosis: without steatosis (WS) of 5% or less (n = 13) and with steatosis (S) of 25% or greater (n = 17). Plasma samples were collected at L1, L2, and 1 day after LT (postoperative [POD]1) for cytokines evaluation. Tissue RNA was isolated for gene expression microarrays. Probeset summaries were obtained using robust multiarray average algorithm. Pairwise comparisons were fit using 2-sample t test. P values 0.01 or less were significant (false discovery rate <5%). Molecular pathway analyses were conducted using Ingenuity Pathway Analysis tool.
resultsSignificantly differentially expressed genes were identified for WS and S grafts after reperfusion. Comprehensive comparison analysis of molecular profiles revealed significant association of S grafts molecular profile with innate immune response activation, macrophage production of nitric oxide and reactive oxygen species, IL-6, IL-8, IL-10 signaling activation, recruitment of granulocytes, and accumulation of myeloid cells. Postreperfusion histological patterns of S grafts revealed neutrophilic infiltration surrounding fat accumulation. Circulating proinflammatory cytokines after reperfusion and 24 hours after LT concurred with intragraft-deregulated molecular pathways. All tested cytokines were significantly increased in plasma of S grafts recipients after reperfusion when compared with WS group at same time.
conclusionsIncreases of graft steatosis exacerbate IRI by exacerbation of innate immune response after LT. Preemptive strategies should consider it for safety usage of steatotic livers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.