Evidence map›Paper›PMID 23593016›Full record

ArticlePLoS genetics2013

Iron-responsive miR-485-3p regulates cellular iron homeostasis by targeting ferroportin.

Carolyn Sangokoya, Jennifer F Doss, Jen-Tsan Chi

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
5.6field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
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  9. Epigenetic regulation of ferroptosis in gastrointestinal cancers (Review).International journal of molecular medicine · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Mechanisms controlling cellular and systemic iron homeostasis.Nature reviews. Molecular cell biology · 2024
    Review
  14. The interplay of miRNAs and ferroptosis in diseases related to iron overload.Apoptosis : an international journal on programmed cell death · 2024
    Review
  15. Review
  16. The role of ferroptosis-related non-coding RNA in liver fibrosis.Frontiers in cell and developmental biology · 2024
    Review
  17. Article
  18. Article
  19. Iron as a therapeutic target in chronic liver disease.World journal of gastroenterology · 2023
    Review
  20. Article

5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Carolyn SangokoyaThe Institute for Genome Sciences and Policy, Duke University School of Medicine, Durham, North Carolina, United States of America.
Jennifer F Doss
Jen-Tsan Chi
Duke University · US

Funding

The Genomic Analysis of Erythrocyte microRNA in Sickle Cell DiseasesR21DK080994 · NIDDK · DUKE UNIVERSITY · PI CHI, JEN-TSAN ASHLEY · 2008 to 2010
$526k
NIDDK NIH HHS R21 DK080994NIDDK NIH HHS R21DK080994
6 · The paper itself

Abstract

Ferroportin (FPN) is the only known cellular iron exporter in mammalian cells and plays a critical role in the maintenance of both cellular and systemic iron balance. During iron deprivation, the translation of FPN is repressed by iron regulatory proteins (IRPs), which bind to the 5' untranslated region (UTR), to reduce iron export and preserve cellular iron. Here, we report a novel iron-responsive mechanism for the post-transcriptional regulation of FPN, mediated by miR-485-3p, which is induced during iron deficiency and represses FPN expression by directly targeting the FPN 3'UTR. The overexpression of miR-485-3p represses FPN expression and leads to increased cellular ferritin levels, consistent with increased cellular iron. Conversely, both inhibition of miR-485-3p activity and mutation of the miR-485-3p target sites on the FPN 3'UTR are able to relieve FPN repression and lead to decreased cellular iron levels. Together, these findings support a model that includes both IRPs and microRNAs as iron-responsive post-transcriptional regulators of FPN. The involvement of microRNA in the iron-responsive regulation of FPN offers additional stability and fine-tuning of iron homeostasis within different cellular contexts. MiR-485-3p-mediated repression of FPN may also offer a novel potential therapeutic mechanism for circumventing hepcidin-resistant mechanisms responsible for some iron overload diseases.

Indexed as

Cation Transport ProteinsIronIron-Regulatory ProteinsMicroRNAsFerroportinGene Expression RegulationHep G2 CellsHomeostasisHumansK562 CellsMutationProtein BindingProtein Processing, Post-TranslationalCation Transport ProteinsFerroportinIronIron-Regulatory ProteinsMicroRNAsMIRN483 microRNA, human

Identifiers

PMID23593016
PMCPMC3616902
OpenAlexW2019610905

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.