ArticlePharmaceuticals (Basel, Switzerland)2019
Deregulation of Hepatic Mek1/2⁻Erk1/2 Signaling Module in Iron Overload Conditions.
Article in Pharmaceuticals (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- FPR1 affects acute rejection in kidney transplantation by regulating iron metabolism in neutrophils.Molecular medicine (Cambridge, Mass.) · 2025Article
- RRP8, associated with immune infiltration, is a prospective therapeutic target in hepatocellular carcinoma.Journal of cancer research and clinical oncology · 2024Article
- Coordination of iron homeostasis by bone morphogenetic proteins: Current understanding and unanswered questions.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Iron as Therapeutic Target in Human Diseases.Pharmaceuticals (Basel, Switzerland) · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The liver, through the production of iron hormone hepcidin, controls body iron levels. High liver iron levels and deregulated hepcidin expression are commonly observed in many liver diseases including highly prevalent genetic iron overload disorders. In spite of a number of breakthrough investigations into the signals that control hepcidin expression, little progress has been made towards investigations into intracellular signaling in the liver under excess of iron. This study examined hepatic signaling pathways underlying acquired and genetic iron overload conditions. Our data demonstrate that hepatic iron overload associates with a decline in the activation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (Erk) kinase (Mek1/2) pathway by selectively affecting the phosphorylation of Erk1/2. We propose that Mek1/2-Erk1/2 signaling is uncoupled from iron-Bmp-Smad-mediated hepcidin induction and that it may contribute to a number of liver pathologies in addition to toxic effects of iron. We believe that our findings will advance the understanding of cellular signaling events in the liver during iron overload of different etiologies.
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Registered trials
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