Evidence map›Paper›PMID 29227331›Full record

ReviewCurrent opinion in clinical nutrition and metabolic care2018

Unravelling new pathways of sterol metabolism: lessons learned from in-born errors and cancer.

Yuqin Wang, William J Griffiths

Open access · hybridAbstract readReview
In one paragraph

Review in Current opinion in clinical nutrition and metabolic care, 2018. 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
3.0field-weighted citation impact, top 9% 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, 16 citations in OpenAlex.

  1. Review
  2. 7-Ketocholesterol: Effects on viral infections and hypothetical contribution in COVID-19.The Journal of steroid biochemistry and molecular biology · 2021
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Sterolomics in biology, biochemistry, medicine.Trends in analytical chemistry : TRAC · 2019
    Review
  8. Oxysterol research: a brief review.Biochemical Society transactions · 2019
    Review
  9. Article
  10. Additional pathways of sterol metabolism: Evidence from analysis of Cyp27a1-/- mouse brain and plasma.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Article
  11. 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

2 authors at 1 institution in 1 country.

Yuqin WangSwansea University Medical School, ILS1 Building, Singleton Park, Swansea, UK.
William J Griffiths
Swansea University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C515771/2Biotechnology and Biological Sciences Research Council BB/I001735/1Biotechnology and Biological Sciences Research Council BB/L001942/1Biotechnology and Biological Sciences Research Council BB/N015932/1
6 · The paper itself

Abstract

purpose of reviewTo update researchers of recently discovered metabolites of cholesterol and of its precursors and to suggest relevant metabolic pathways. RECENT

findingsPatients suffering from inborn errors of sterol biosynthesis, transport and metabolism display unusual metabolic pathways, which may be major routes in the diseased state but minor in the healthy individual. Although quantitatively minor, these pathways may still be important in healthy individuals. Four inborn errors of metabolism, Smith-Lemli-Opitz syndrome, cerebrotendinous xanthomatosis and Niemann Pick disease types B (NPB) and C (NPC) result from mutations in different genes but can generate elevated levels of the same sterol metabolite, 7-oxocholesterol, in plasma. How this molecule is metabolized further is of great interest as its metabolites may have an important role in embryonic development. A second metabolite, abundant in NPC and NPB diseases, cholestane-3β,5α,6β-triol (3β,5α,6β-triol), has recently been shown to be metabolized to the corresponding bile acid, 3β,5α,6β-trihydroxycholanoic acid, providing a diagnostic marker in plasma. The origin of cholestane-3β,5α,6β-triol is likely to be 3β-hydroxycholestan-5,6-epoxide, which can alternatively be metabolized to the tumour suppressor dendrogenin A (DDA). In breast tumours, DDA levels are found to be decreased compared with normal tissues linking sterol metabolism to cancer. SUMMARY: Unusual sterol metabolites and pathways may not only provide markers of disease, but also clues towards cause and treatment.

Indexed as

BiomarkersBreast NeoplasmsCholestanolsHumansImidazolesKetocholesterolsLipid MetabolismNiemann-Pick Disease, Type BNiemann-Pick Disease, Type CSmith-Lemli-Opitz SyndromeSterolsXanthomatosis, Cerebrotendinous5-hydroxy-6-(2-(1H-imidazol-4-yl)ethylamino)cholestan-3-ol7-ketocholesterolBiomarkersCholestanolsImidazolesKetocholesterolsSterols

Identifiers

PMID29227331
PMCPMC5808834
OpenAlexW2775337332

What OpenQuestion 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 OpenQuestion graph.