Evidence map›Paper›PMID 34367715›Full record

ArticleLiver research (Beijing, China)2017

New insights into the role of

Helen H Wang, Tiangang Li, Piero Portincasa, David A Ford, Brent A Neuschwander-Tetri, Patrick Tso, David Q-H Wang

Open access · goldAbstract read
In one paragraph

Article in Liver research (Beijing, China), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Genetics of Gallstone Disease and Their Clinical Significance: A Narrative Review.Journal of clinical and translational hepatology · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Genetic Analysis ofGenes · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Physical Activity Modulating Lipid Metabolism in Gallbladder Diseases.Journal of gastrointestinal and liver diseases : JGLD · 2020
    Review
  18. Review
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

7 authors at 4 institutions in 2 countries.

Helen H WangDepartment of Internal Medicine, Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Tiangang LiDepartment of Pharmacology, Toxicology and Therapeutics, Kansas University Medical Center, Kansas City, KS, USA.
Piero PortincasaClinica Medica "A. Murri", Department of Biomedical Sciences and Human Oncology, University of Bari "Aldo Moro"Medical School, Bari, Italy.
David A FordDepartment of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Brent A Neuschwander-TetriDepartment of Internal Medicine, Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Patrick TsoDepartment of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
David Q-H WangDepartment of Internal Medicine, Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Saint Louis University · USUniversity of Bari Aldo Moro · ITUniversity of Cincinnati Medical Center · USUniversity of Kansas Medical Center · US

Funding

GPR30 and Hepatic Cholesterol HomeostasisR01DK106249 · NIDDK · SAINT LOUIS UNIVERSITY · PI WANG, DAVID Q · 2015 to 2017
$1.0M
Role of GPR30 in Hepatic Lipid MetabolismR56DK101793 · NIDDK · SAINT LOUIS UNIVERSITY · PI WANG, DAVID Q · 2014 to 2014
$189k
NIDDK NIH HHS R01 DK106249NIDDK NIH HHS R56 DK101793
6 · The paper itself

Abstract

Cholesterol gallstone formation represents a failure of biliary cholesterol homeostasis in which the physical-chemical balance of cholesterol solubility in bile is disturbed. Lithogenic bile is mainly caused by persistent hepatic hypersecretion of biliary cholesterol and sustained cholesterol-supersaturated bile is an essential prerequisite for the precipitation of solid cholesterol monohydrate crystals and the formation of cholesterol gallstones. The metabolic determinants of the supply of hepatic cholesterol molecules that are recruited for biliary secretion are dependent upon the input-output balance of cholesterol and its catabolism in the liver. The sources of cholesterol for hepatic secretion into bile have been extensively investigated; however, to what extent each cholesterol source contributes to hepatic secretion is still unclear both under normal physiological conditions and in the lithogenic state. Although it has been long known that biliary lithogenicity is initiated by hepatic cholesterol hypersecretion, the genetic mechanisms that cause supersaturated bile have not been defined yet. Identification of the

Indexed as

Bile acidBile flowBiliary secretionLith geneMicelleVesicle

Identifiers

PMID34367715
PMCPMC8341472
OpenAlexW2620803792

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.