ReviewFrontiers in immunology2022
Reactive Oxygen Species Induce Fatty Liver and Ischemia-Reperfusion Injury by Promoting Inflammation and Cell Death.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.
What it found
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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
106 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.
- Effects of carotenoid supplementation on liver enzymes in adults: a GRADE-assessed systematic review and dose-response meta-analysis of randomized controlled trials.BMC complementary medicine and therapies · 2025Pooled it
- Protective Efficiency Comparison of Direct and Remote Ischemic Preconditioning on Ischemia Reperfusion Injury of the Liver in Patients Undergoing Partial Hepatectomy.BioMed research international · 2023Trial
- Reactive oxygen species (ROS) research in drug discovery and drug delivery: Can the medium Be a Trojan Horse disguised as something benign?Journal of enzyme inhibition and medicinal chemistry · 2026Article
- CO-mediated restoration of mitochondrial redox homeostasis contributes to alleviating multiple programmed cell deaths in hepatic I/R injury.Redox biology · 2026Article
- Endothelial dysfunction: A central mechanism linking autosomal dominant polycystic kidney disease and intracranial aneurysms (Review).International journal of molecular medicine · 2026Review
- Threshold-based association between controlled attenuation parameter-defined hepatic steatosis and hepatectomy-associated ischemia-reperfusion injury: A retrospective cohort study.The Journal of international medical research · 2026Article
- Succinate and lactate produced as conserved biomarkers through chronic and transient substrate-level phosphorylation: from microorganisms to cancer.Journal of bioenergetics and biomembranes · 2026Review
- Design and evaluation of peroxiredoxin 1 agonist based on scaffold hopping of salvianolic acids and combinatorial click chemistry.Acta pharmacologica Sinica · 2026Article
- Article
- RT-qPCR-based transcriptional profiling of the effects of tarantula logoplex on inflammatory, oxidative stress and apoptosis pathways in remote organs in experimental lower extremity ischemia-reperfusion injury.Molecular biology reports · 2026Article
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- Hydrogen gas with hypothermic machine perfusion induces lipidomic alterations in donation-after-cardiac-death rat livers.Journal of lipid research · 2026Article
- Resveratrol-loaded chitosan nanoparticles and adipose-derived stem cell-conditioned medium for liver protection against ischemia-reperfusion injury.Journal of materials science. Materials in medicine · 2026Article
- Mg/Mn bi-single-atom carbon dot nanozymes with enhanced SOD-like activity and fluorescence for hepatoprotection.Journal of nanobiotechnology · 2026Article
- Mitochondrial DNA regulation of hepatic ischemia-reperfusion injury and intervention strategies.Journal of translational medicine · 2026Review
- Oxidative Stress, Environmental Pollutants, Aging, and Epigenetic Regulation: Mechanistic Insights and Biomarker Advances.Antioxidants (Basel, Switzerland) · 2026Review
- The Mechanism of G Protein-Coupled Receptor Regulation of Ferroptosis in Hepatic Ischemia-Reperfusion Injury.International journal of molecular sciences · 2026Review
- Inferior Long-Term Outcome of Fatty Liver Allografts After Orthotopic Liver Transplantation.Annals of transplantation · 2026Article
- TM9SF1 Aggravates Liver Ischemia-Reperfusion Injury by Promoting Autophagy.Inflammation · 2026Article
- Procyanidin B2 and an autochthonous apple pulp extract modulate oxidative stress and PPARγ expression on an in vitro model of lipid steatosis in HepG2 cells.Journal of physiology and biochemistry · 2026Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver transplantation is the ultimate method for treating end-stage liver disease. With the increasing prevalence of obesity, the number of patients with non-alcoholic fatty liver, a common cause of chronic liver disease, is on the rise and may become the main cause of liver transplantation in the future. With the increasing gap between the number of donor livers and patients waiting for liver transplantation and the increasing prevalence of non-alcoholic fatty liver, the proportion of steatosis livers among non-standard donor organs is also increasing. Ischemia-reperfusion injury has historically been the focus of attention in the liver transplantation process, and severe ischemia-reperfusion injury leads to adverse outcomes of liver transplantation. Studies have shown that the production of reactive oxygen species and subsequent oxidative stress play a key role in the pathogenesis of hepatic ischemia and reperfusion injury and non-alcoholic fatty liver. Furthermore, the sensitivity of fatty liver transplantation to ischemia-reperfusion injury has been suggested to be related to the production of reactive oxygen species (ROS) and oxidative stress. In ischemia-reperfusion injury, Kupffer cell and macrophage activation along with mitochondrial damage and the xanthine/xanthine oxidase system promote marked reactive oxygen species production and the inflammatory response and apoptosis, resulting in liver tissue injury. The increased levels of ROS and lipid peroxidation products, vicious circle of ROS and oxidative stress along with mitochondrial dysfunction promoted the progress of non-alcoholic fatty liver. In contrast to the non-fatty liver, a non-alcoholic fatty liver produces more reactive oxygen species and suffers more serious oxidative stress when subjected to ischemia-reperfusion injury. We herein review the effects of reactive oxygen species on ischemia-reperfusion injury and non-alcoholic fatty liver injury as well as highlight several treatment approaches.
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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.