ArticleScientific reports2018
Iron-Overload triggers ADAM-17 mediated inflammation in Severe Alcoholic Hepatitis.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Impact of Sappan Wood Extract as Iron Chelator Adjuvant on Iron Concentration and Macrophage Polarization in Rat Spleen.Iranian journal of medical sciences · 2025Article
- Implications for soluble iron accumulation, oxidative stress, and glial glutamate release in motor neuron death associated with sporadic amyotrophic lateral sclerosis.Neuropathology : official journal of the Japanese Society of Neuropathology · 2025Review
- Molecular mechanisms of alcohol-associated liver disease-ferroptosis and autophagy crosstalk.Molecular biology reports · 2025Review
- GAS6/TAM Axis as Therapeutic Target in Liver Diseases.Seminars in liver disease · 2024Article
- Iron and copper: critical executioners of ferroptosis, cuproptosis and other forms of cell death.Cell communication and signaling : CCS · 2023Review
- The immunological role of ADAMs in the field of gastroenterological chronic inflammatory diseases and cancers: a review.Oncogene · 2023Review
- Iron as a therapeutic target in chronic liver disease.World journal of gastroenterology · 2023Review
- Obese Patients With Nonalcoholic Fatty Liver Disease Have an Increase in Soluble Plasma CD163 and a Concurrent Decrease in Hepatic Expression of CD163.Gastro hep advances · 2023Article
- Targeting ferroptosis, a novel programmed cell death, for the potential of alcohol-related liver disease therapy.Frontiers in pharmacology · 2023Review
- The Importance of Nutraceuticals in COVID-19: What's the Role of Resveratrol?Molecules (Basel, Switzerland) · 2022Review
- Non-heme iron overload impairs monocyte to macrophage differentiationFrontiers in immunology · 2022Article
- Contributing factors common to COVID‑19 and gastrointestinal cancer.Oncology reports · 2022Review
- Red Blood Cell-Derived Iron Alters Macrophage Function in COPD.Biomedicines · 2021Article
- Role of NRF2 and Sirtuin activators in COVID-19.Clinical immunology (Orlando, Fla.) · 2021Review
- From Anti-SARS-CoV-2 Immune Response to the Cytokine Storm via Molecular Mimicry.Antibodies (Basel, Switzerland) · 2021Article
- Redox-Active Metal Ions and Amyloid-Degrading Enzymes in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- ADAM and ADAMTS Proteins, New Players in the Regulation of Hepatocellular Carcinoma Microenvironment.Cancers · 2021Review
- COVID-19: NADMedical hypotheses · 2020Article
- Neutrophils from hereditary hemochromatosis patients are protected from iron excess and are primed.Blood advances · 2020Article
- Targeting of CD163International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Severe alcoholic hepatitis (SAH) is associated with iron accumulation in hepatocytes/macrophages. This possibly correlates with inflammation and stress but the exact mechanism still remains obscure. To understand the role of iron and the mechanisms of systemic iron-overload, a transcriptomic study of liver and Peripheral Blood -Mononuclear-Cells (PBMCs) was undertaken in SAH patients, with and without hepatic iron-overload. Our results show that iron-overload in hepatocytes/macrophages is due to an increased expression of iron-loading receptors and CD163 signaling cascade. Increase in labile iron pool induces expression of iron-loading, oxidative-stress and inflammatory genes along with expression of CD163 and ADAM17. Increased liver iron correlated with circulatory iron, TNF-α, macrophage activation (sCD163) and peroxide-stress in CD163
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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.