Evidence map›Paper›PMID 33707579›Full record

ArticleScientific reports2021

Systemic deletion of Atp7b modifies the hepatocytes' response to copper overload in the mouse models of Wilson disease.

Abigael Muchenditsi, C Conover Talbot, Aline Gottlieb, Haojun Yang, Byunghak Kang, Tatiana Boronina, Robert Cole, Li Wang, Som Dev, James P Hamilton and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. 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
5.1field-weighted citation impact, top 4% 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, 51 citations in OpenAlex.

  1. Article
  2. Metallothionein and neurodegenerative diseases.Neural regeneration research · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Hepatic oxylipin profiles in mouse models of Wilson disease: New insights into early hepatic manifestations.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. α-lipoic acid ameliorates consequences of copper overload by up-regulating selenoproteins and decreasing redox misbalance.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Article
  19. Mitochondrial copper in human genetic disorders.Trends in endocrinology and metabolism: TEM · 2023
    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

11 authors at 1 institution in 1 country.

Abigael MuchenditsiDepartment of Physiology, Johns Hopkins Medical Institutes, 725 N Wolfe street, Baltimore, MD, 21205, USA.
C Conover TalbotCore Analysis Unit, Johns Hopkins Medical Institutes, Baltimore, MD, 21205, USA.
Aline GottliebDepartment of Physiology, Johns Hopkins Medical Institutes, 725 N Wolfe street, Baltimore, MD, 21205, USA.
Haojun YangDepartment of Physiology, Johns Hopkins Medical Institutes, 725 N Wolfe street, Baltimore, MD, 21205, USA.
Byunghak KangDepartment of Molecular and Comparative Pathobiology, Johns Hopkins Medical Institutes, Baltimore, MD, 21205, USA.
Tatiana BoroninaMass Spectrometry and Proteomics Facility, Johns Hopkins Medical Institutes, Baltimore, MD, 21205, USA.
Robert ColeMass Spectrometry and Proteomics Facility, Johns Hopkins Medical Institutes, Baltimore, MD, 21205, USA.
Li WangDepartment of Physiology, Johns Hopkins Medical Institutes, 725 N Wolfe street, Baltimore, MD, 21205, USA.
Som DevDepartment of Physiology, Johns Hopkins Medical Institutes, 725 N Wolfe street, Baltimore, MD, 21205, USA.
James P HamiltonDepartment of Medicine, Johns Hopkins Medical Institutes, Baltimore, MD, 21205, USA.
Svetlana LutsenkoDepartment of Physiology, Johns Hopkins Medical Institutes, 725 N Wolfe street, Baltimore, MD, 21205, USA. lutsenko@jhmi.edu.
Johns Hopkins University · US

Funding

Copper Homeostasis and Liver FunctionR01DK117396 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI JAMES P HAMILTON, SVETLANA LUTSENKO · 2018 to 2026
$3.9M
NIDDK NIH HHS R01 DK117396
6 · The paper itself

Abstract

Wilson disease (WD) is caused by inactivation of the copper transporter Atp7b and copper overload in tissues. Mice with Atp7b deleted either globally (systemic inactivation) or only in hepatocyte recapitulate various aspects of human disease. However, their phenotypes vary, and neither the common response to copper overload nor factors contributing to variability are well defined. Using metabolic, histologic, and proteome analyses in three Atp7b-deficient mouse strains, we show that global inactivation of Atp7b enhances and specifically modifies the hepatocyte response to Cu overload. The loss of Atp7b only in hepatocytes dysregulates lipid and nucleic acid metabolisms and increases the abundance of respiratory chain components and redox balancing enzymes. In global knockouts, independently of their background, the metabolism of lipid, nucleic acid, and amino acids is inhibited, respiratory chain components are down-regulated, inflammatory response and regulation of chromosomal replication are enhanced. Decrease in glucokinase and lathosterol oxidase and elevation of mucin-13 and S100A10 are observed in all Atp7b mutant strains and reflect the extent of liver injury. The magnitude of proteomic changes in Atp7b

Indexed as

Gene DeletionAnimalsBiomarkersCopperCopper-Transporting ATPasesDisease Models, AnimalGlucoseGlycogenHepatocytesHepatolenticular DegenerationLipid MetabolismLiverMiceMice, Inbred C57BLMice, KnockoutPhenotypeATP7B protein, humanBiomarkersCopperCopper-Transporting ATPasesGlucoseGlycogenProteome

Identifiers

PMID33707579
PMCPMC7952580
OpenAlexW3134846705

What Socratic holds

Textmetadata
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 Socratic graph.