Evidence map›Paper›PMID 29728459›Full record

ReviewJournal of lipid research2018

ABCG5 and ABCG8: more than a defense against xenosterols.

Shailendra B Patel, Gregory A Graf, Ryan E Temel

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
11.8field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
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  11. Article
  12. Article
  13. Article
  14. Cerebral involvement in sitosterolemia.Lipids in health and disease · 2024
    Article
  15. The desert woodrat (Neotoma lepida) induces a diversity of biotransformation genes in response to creosote bush resin.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2024
    Article
  16. Article
  17. Association of ABCG5 and ABCG8 Transporters with Sitosterolemia.Advances in experimental medicine and biology · 2024
    Review
  18. Exploring endocrine FGFs - structures, functions and biomedical applications.International journal of biochemistry and molecular biology · 2024
    Review
  19. Article
  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.

Shailendra B PatelDivision of Endocrinology, Diabetes, and Metabolism, University of Cincinnati, Cincinnati, OH 45219 sbpatel@uc.edu Gregory.graf@uky.edu ryan.temel@uky.edu.ORCID 0000-0003-0046-5513
Gregory A GrafDepartment of Pharmaceutical Sciences and Saha Cardiovascular Research Center and University of Kentucky, Lexington, KY 40536 sbpatel@uc.edu Gregory.graf@uky.edu ryan.temel@uky.edu.ORCID 0000-0002-0130-9929
Ryan E TemelDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY 40536 sbpatel@uc.edu Gregory.graf@uky.edu ryan.temel@uky.edu.ORCID 0000-0002-9599-804X
University of Kentucky · USUniversity of Cincinnati · US

Funding

Contributions of Hepatic and Intestinal Pathways to Cholesterol ExcretionR01DK113625 · NIDDK · UNIVERSITY OF KENTUCKY · PI Gregory A Graf · 2017 to 2026
$4.2M
NIDDK NIH HHS R01 DK113625
6 · The paper itself

Abstract

The elucidation of the molecular basis of the rare disease, sitosterolemia, has revolutionized our mechanistic understanding of how dietary sterols are excreted and how cholesterol is eliminated from the body. Two proteins, ABCG5 and ABCG8, encoded by the sitosterolemia locus, work as obligate dimers to pump sterols out of hepatocytes and enterocytes. ABCG5/ABCG8 are key in regulating whole-body sterol trafficking, by eliminating sterols via the biliary tree as well as the intestinal tract. Importantly, these transporters keep xenosterols from accumulating in the body. The sitosterolemia locus has been genetically associated with lipid levels and downstream atherosclerotic disease, as well as formation of gallstones and the risk of gallbladder cancer. While polymorphic variants raise or lower the risks of these phenotypes, loss of function of this locus leads to more dramatic phenotypes, such as premature atherosclerosis, platelet dysfunction, and thrombocytopenia, and, perhaps, increased endocrine disruption and liver dysfunction. Whether small amounts of xenosterol exposure over a lifetime cause pathology in normal humans with polymorphic variants at the sitosterolemia locus remains largely unexplored. The purpose of this review will be to summarize the current state of knowledge, but also highlight key conceptual and mechanistic issues that remain to be explored.

Indexed as

AnimalsATP Binding Cassette Transporter, Subfamily G, Member 5ATP Binding Cassette Transporter, Subfamily G, Member 8HumansSterolsATP Binding Cassette Transporter, Subfamily G, Member 5ATP Binding Cassette Transporter, Subfamily G, Member 8SterolsatherosclerosisATP binding cassette transporter G5ATP binding cassette transporter G8bilecholesterolmacrothrombocytopeniaphytosterolsplateletssitosterolemia

Identifiers

PMID29728459
PMCPMC6027916
OpenAlexW2800441475

What OpenQuestion holds

Textmetadata
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.