ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
Hepatic macrophage iron aggravates experimental alcoholic steatohepatitis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Macrophage heterogeneity in liver fibrosis.Frontiers in immunology · 2025Review
- Liver Iron Loading in Alcohol-Associated Liver Disease.The American journal of pathology · 2023Review
- Mitochondrial Dysfunction: At the Nexus between Alcohol-Associated Immunometabolic Dysregulation and Tissue Injury.International journal of molecular sciences · 2023Review
- Targeting ferroptosis, a novel programmed cell death, for the potential of alcohol-related liver disease therapy.Frontiers in pharmacology · 2023Review
- Iron overload in alcoholic liver disease: underlying mechanisms, detrimental effects, and potential therapeutic targets.Cellular and molecular life sciences : CMLS · 2022Review
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
- Recent Insights Into the Role of Immune Cells in Alcoholic Liver Disease.Frontiers in immunology · 2019Review
- Knockout of microRNA-21 attenuates alcoholic hepatitis through the VHL/NF-κB signaling pathway in hepatic stellate cells.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Regulation of Cellular Senescence by miR-34a in Alcoholic Liver Injury.The American journal of pathology · 2017Article
- Effect of iron on cholesterol 7α-hydroxylase expression in alcohol-induced hepatic steatosis in mice.Journal of lipid research · 2017Article
- Metabolic reprogramming and cell fate regulation in alcoholic liver disease.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2015Review
- Iron Toxicity in the Retina Requires Alu RNA and the NLRP3 Inflammasome.Cell reports · 2015Article
- Alcoholic liver disease: mechanisms of injury and targeted treatment.Nature reviews. Gastroenterology & hepatology · 2015Review
- Effects of combined alcohol and anti-HIV drugs on cellular stress responses in primary hepatocytes and hepatic stellate and kupffer cells.Alcoholism, clinical and experimental research · 2015Article
- Regulation of the extrinsic apoptotic pathway by microRNA-21 in alcoholic liver injury.The Journal of biological chemistry · 2014Article
- New advances in molecular mechanisms and emerging therapeutic targets in alcoholic liver diseases.World journal of gastroenterology · 2014Review
- Kupffer cells in the liver.Comprehensive Physiology · 2013Review
- Increased iron loading induces Bmp6 expression in the non-parenchymal cells of the liver independent of the BMP-signaling pathway.PloS one · 2013Article
- Caveosomal oxidative stress causes Src-p21ras activation and lysine 63 TRAF6 protein polyubiquitination in iron-induced M1 hepatic macrophage activation.The Journal of biological chemistry · 2012Article
- Epigenetic regulation of miR-34a expression in alcoholic liver injury.The American journal of pathology · 2012Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
One prime feature of alcoholic liver disease (ALD) is iron accumulation in hepatic macrophages/Kupffer cells (KC) associated with enhanced NF-kappaB activation. Our recent work demonstrates a peroxynitrite-mediated transient rise in intracellular labile iron (ILI) as novel signaling for endotoxin-induced IKK and NF-kappaB activation in rodent KC. The present study investigated the mechanism of KC iron accumulation and its effects on ILI response in experimental ALD. We also tested ILI response in human blood monocytes. Chronic alcohol feeding in rats results in increased expression of transferrin (Tf) receptor-1 and hemochromatosis gene (HFE), enhanced iron uptake, an increase in nonheme iron content, and accentuated ILI response for NF-kappaB activation in KC. Ex vivo treatment of these KC with an iron chelator abrogates the increment of iron content, ILI response, and NF-kappaB activation. The ILI response is evident in macrophages derived from human blood monocytes by PMA treatment but not in vehicle-treated monocytes, and this differentiation-associated phenomenon is essential for maximal TNF-alpha release. PMA-induced macrophages load iron dextran and enhance ILI response and TNF-alpha release. These effects are reproduced in KC selectively loaded in vivo with iron dextran in mice and more importantly aggravate experimental ALD. Our results suggest enhanced iron uptake as a mechanism of KC iron loading in ALD and demonstrate the ILI response as a function acquired by differentiated macrophages in humans and as a priming mechanism for ALD.
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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.