Evidence map›Paper›PMID 37741465›Full record

ReviewPharmacology & therapeutics2023

Therapeutic implications of impaired nuclear receptor function and dysregulated metabolism in Wilson's disease.

Clavia Ruth Wooton-Kee

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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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

1 author at 1 institution in 1 country.

Clavia Ruth Wooton-KeeBaylor College of Medicine, Department of Pediatrics-Nutrition, Children's Nutrition Research Center, Houston, TX, United States of America. Electronic address: wootenke@bcm.edu.
Children's Nutrition Research Center at Baylor College of Medicine · US

Funding

Nuclear Receptor Dysfunction Reprograms Metabolism and Cellular Proliferation in Wilson's DiseaseR01DK129579 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI Clavia Ruth Wooton-Kee · 2022 to 2026
$1.6M
Nuclear Receptors as Novel Therapeutic Targets for Wilson’s DiseaseK01DK111716 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI WOOTON-KEE, CLAVIA RUTH · 2017 to 2021
$746k
Excessive Copper Levels Disrupt Hepatic Nuclear Receptor FunctionF32DK089689 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI WOOTON-KEE, CLAVIA RUTH · 2010 to 2011
$65k
NIDDK NIH HHS F32 DK089689NIDDK NIH HHS K01 DK111716NIDDK NIH HHS R01 DK129579
6 · The paper itself

Abstract

Copper is an essential trace element that is required for the activity of many enzymes and cellular processes, including energy homeostasis and neurotransmitter biosynthesis; however, excess copper accumulation results in significant cellular toxicity. The liver is the major organ for maintaining copper homeostasis. Inactivating mutations of the copper-transporting P-type ATPase, ATP7B, result in Wilson's disease, an autosomal recessive disorder that requires life-long medicinal therapy or liver transplantation. Current treatment protocols are limited to either sequestration of copper via chelation or reduction of copper absorption in the gut (zinc therapy). The goal of these strategies is to reduce free copper, redox stress, and cellular toxicity. Several lines of evidence in Wilson's disease animal models and patients have revealed altered hepatic metabolism and impaired hepatic nuclear receptor activity. Nuclear receptors are transcription factors that coordinate hepatic metabolism in normal and diseased livers, and several hepatic nuclear receptors have decreased activity in Wilson's disease and Atp7b

Indexed as

Hepatolenticular DegenerationAnimalsCopperHumansLiverReceptors, Cytoplasmic and NuclearZincCopperReceptors, Cytoplasmic and NuclearZincCopperLiverMetabolismNuclear receptorsWilson's disease

Identifiers

PMID37741465
PMCPMC10841433
OpenAlexW4386968479

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.