ArticleHepatology (Baltimore, Md.)2009
Age-related decrease in proteasome expression contributes to defective nuclear factor-kappaB activation during hepatic ischemia/reperfusion.
Article in Hepatology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- 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
- Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Impact of age on liver damage, inflammation, and molecular signaling pathways in response to femoral fracture and hemorrhage.Frontiers in immunology · 2023Article
- Review
- 1,4-dihydropyridine derivatives increase mRNA expression ofArhiv za higijenu rada i toksikologiju · 2021Article
- Liver Ischemia Reperfusion Injury, Enhanced by Trained Immunity, Is Attenuated in Caspase 1/Caspase 11 Double Gene Knockout Mice.Pathogens (Basel, Switzerland) · 2020Article
- miR-219a-5p Ameliorates Hepatic Ischemia/Reperfusion Injury via Impairing TP53BP2.Digestive diseases and sciences · 2019Article
- Impaired capacity to restore proteostasis in the aged brain after ischemia: Implications for translational brain ischemia research.Neurochemistry international · 2019Review
- Identification of Key Transcription Factors AP-1 and AP-1-Dependent miRNAs Forming a Co-Regulatory Network Controlling PTEN in Liver Ischemia/Reperfusion Injury.BioMed research international · 2019Article
- Proteasome and Organs Ischemia-Reperfusion Injury.International journal of molecular sciences · 2017Review
- Study of the protective effect of ischemic and pharmacological preconditioning on hepatic ischemic reperfusion injury induced in rats.JGH open : an open access journal of gastroenterology and hepatology · 2017Article
- Gene microarray analysis of expression profiles in liver ischemia and reperfusion.Molecular medicine reports · 2017Article
- Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury.BioMed research international · 2015Review
- Molecular alterations in proteasomes of rat liver during aging result in altered proteolytic activities.Age (Dordrecht, Netherlands) · 2014Article
- Molecular signatures of mammalian hibernation: comparisons with alternative phenotypes.BMC genomics · 2013Article
- Functions of autophagy in normal and diseased liver.Autophagy · 2013Review
- Negative regulation of 26S proteasome stability via calpain-mediated cleavage of Rpn10 subunit upon mitochondrial dysfunction in neurons.The Journal of biological chemistry · 2013Article
- Ubiquitin-proteasome system inhibitors and AMPK regulation in hepatic cold ischaemia and reperfusion injury: possible mechanisms.Clinical science (London, England : 1979) · 2012Article
- Association analyses suggest the effects of RANK and RANKL on age at menarche in Chinese women.Climacteric : the journal of the International Menopause Society · 2012Article
- Effects and mechanisms of store-operated calcium channel blockade on hepatic ischemia-reperfusion injury in rats.World journal of gastroenterology · 2012Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatic ischemia/reperfusion (I/R) leads to liver injury and dysfunction through the initiation of a biphasic inflammatory response that is regulated by the transcription factor nuclear factor kappaB (NF-kappaB). We have previously shown that there is an age-dependent difference in the injury response to hepatic I/R in mice that correlates with divergent activation of NF-kappaB such that young mice have greater NF-kappaB activation, but less injury than old mice. In this study, we investigated the mechanism by which age alters the activation of NF-kappaB in the liver during I/R. Young (4-5 weeks) and old (12-14 months) mice underwent partial hepatic I/R. Livers were obtained for RNA microarray analysis and protein expression assays. Using microarray analysis, we identified age-dependent differences in the expression of genes related to protein ubiquitinylation and the proteasome. In old mice, genes that are involved in the ubiquitin-proteasome pathway were significantly down-regulated during I/R. Consistent with these findings, expression of a critical proteasome subunit, non-adenosine triphosphatase 4 (PSMD4), was reduced in old mice. Expression of the NF-kappaB inhibitory protein, IkappaB alpha, was increased in old mice and was greatly phosphorylated and ubiquitinylated. The data provide strong evidence that the age-related defect in hepatic NF-kappaB signaling during I/R is a result of decreased expression of PSMD4, a proteasome subunit responsible for recognition and recruitment of ubiquitinylated substrates to the proteasome. It appears that decreased PSMD4 expression prevents recruitment of phosphorylated and ubiquitinylated IkappaB alpha to the proteasome, resulting in a defect in NF-kappaB activation.
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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.