ArticleBlood cells, molecules & diseases2014
A chemical screen identifies small molecules that regulate hepcidin expression.
Article in Blood cells, molecules & diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Pooled it
- The Interplay Between Endoplasmic Reticulum Stress and Ferroptosis in Neurological Diseases.Neurochemical research · 2025Review
- A high-throughput screening to identify small molecules that suppress huntingtin promoter activity or activate huntingtin-antisense promoter activity.Scientific reports · 2021Article
- Ferroptosis and Its Multifaceted Roles in Cerebral Stroke.Frontiers in cellular neuroscience · 2021Review
- [Progress on epigenetic regulation of iron homeostasis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
- Therapeutic Advances in Regulating the Hepcidin/Ferroportin Axis.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Hepcidin Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Hepcidin is regulated by promoter-associated histone acetylation and HDAC3.Nature communications · 2017Article
- Imatinib and spironolactone suppress hepcidin expression.Haematologica · 2017Article
- Anemia of Inflammation: A Review.The Medical clinics of North America · 2017Review
- Dietary supplementation with ipriflavone decreases hepatic iron stores in wild type mice.Blood cells, molecules & diseases · 2016Article
- Pharmacological Targeting of the Hepcidin/Ferroportin Axis.Frontiers in pharmacology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Hepcidin, a peptide hormone produced in the liver, decreases intestinal iron absorption and macrophage iron release via effects on ferroportin. Bone morphogenic protein and Stat3 signaling regulate Hepcidin's transcription. Hepcidin is a potential drug target for patients with iron overload syndromes because its levels are inappropriately low in these individuals. To generate a tool for identifying small molecules that modulate Hepcidin expression, we stably transfected human hepatocytes (HepG2) cells with a reporter construct containing 2.7kb of the human Hepcidin promoter upstream of a firefly reporter gene. We used high throughput methods to screen 10,169 chemicals in duplicate for their effect on Hepcidin expression and cell viability. Regulators were identified as chemicals that caused a change >3 standard deviations above or >1 standard deviation below the mean of the other chemicals (z-score >3 or <1), while not adversely affecting cell viability, quantified by fluorescence assay. Following validation assays, we identified 16 chemicals in a broad range of functional classes that promote Hepcidin expression. All of the chemicals identified increased expression of bone morphogenic protein-dependent and/or Stat3-dependent genes, however none of them strongly increased phosphorylation of Smad1,5,8 or Stat3.
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What OpenQuestion holds
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.