Evidence map›Paper›PMID 21380607›Full record

ReviewBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine2011

Systems biology approach to Wilson's disease.

Jason L Burkhead, Lawrence W Gray, Svetlana Lutsenko

Abstract readReview
In one paragraph

Review in Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. [Progress on the research of hepatolenticular degeneration].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. InfantileJPGN reports · 2021
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Altered zinc balance in the Atp7bMetallomics : integrated biometal science · 2018
    Article
  14. Copper Exposure Perturbs Brain Inflammatory Responses and Impairs Clearance of Amyloid-Beta.Toxicological sciences : an official journal of the Society of Toxicology · 2016
    Article
  15. Article
  16. Article
  17. Wilson's disease: a comprehensive review of the molecular mechanisms.International journal of molecular sciences · 2015
    Review
  18. Review
  19. Review
  20. Article
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 2 institutions in 1 country.

Jason L BurkheadUniversity of Alaska Anchorage, Anchorage, AK 99508, USA.
Lawrence W Gray
Svetlana Lutsenko
Johns Hopkins University · USUniversity of Alaska Anchorage · US

Funding

VIROLOGISTP20RR016466 · NCRR · UNIVERSITY OF ALASKA FAIRBANKS · PI KREBS, JOCELYN E · 2001 to 2011
$37.0M
The role of transferrin receptor 2 in iron homeostasisP01GM067166 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BLACKBURN, NINIAN J · 2003 to 2013
$14.6M
Characterization of nuclear proteome in normal and diseased liverR21DK075659 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI LUTSENKO, SVETLANA · 2006 to 2007
$379k
Mechanisms of Homeostatic Control of Copper in TissuesF31DK084730 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI GRAY, LAWRENCE WILSON · 2009 to 2011
$124k
NCRR NIH HHS P20 RR016466NCRR NIH HHS P20RR016466-10NIDDK NIH HHS F31 DK084730NIDDK NIH HHS F31DK084730-02NIDDK NIH HHS R21 DK075659NIGMS NIH HHS P01 GM067166
6 · The paper itself

Abstract

Wilson's disease (WD) is a severe disorder of copper misbalance, which manifests with a wide spectrum of liver pathology and/or neurologic and psychiatric symptoms. WD is caused by mutations in a gene encoding a copper-transporting ATPase ATP7B and is accompanied by accumulation of copper in tissues, especially in the liver. Copper-chelation therapy is available for treatment of WD symptoms and is often successful, however, significant challenges remain with respect to timely diagnostics and treatment of the disease. The lack of genotype-phenotype correlation remains unexplained, the causes of fulminant liver failure are not known, and the treatment of neurologic symptoms is only partially successful, underscoring the need for better understanding of WD mechanisms and factors that influence disease manifestations. Recent gene and protein profiling studies in animal models of WD began to uncover cellular processes that are primarily affected by copper accumulation in the liver. The results of such studies, summarized in this review, revealed new molecular players and pathways (cell cycle and cholesterol metabolism, mRNA splicing and nuclear receptor signaling) linked to copper misbalance. A systems biology approach promises to generate a comprehensive view of WD onset and progression, thus helping with a more fine-tune treatment and monitoring of the disorder.

Indexed as

Systems BiologyAdenosine TriphosphatasesAnimalsCation Transport ProteinsCopperCopper-Transporting ATPasesDisease Models, AnimalGene Regulatory NetworksGenetic Association StudiesHepatolenticular DegenerationHumansMutationPhenotypeSignal TransductionAdenosine TriphosphatasesATP7B protein, humanCation Transport ProteinsCopperCopper-Transporting ATPases

Identifiers

PMID21380607
PMCPMC3106420
OpenAlexW1977972524

What OpenQuestion holds

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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.