Evidence map›Paper›PMID 24302009›Full record

ReviewAmerican journal of physiology. Endocrinology and metabolism2014

Sulfation of 25-hydroxycholesterol regulates lipid metabolism, inflammatory responses, and cell proliferation.

Shunlin Ren, Yanxia Ning

Abstract readReview
In one paragraph

Review in American journal of physiology. Endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 58 citations in OpenAlex.

  1. Discovery of a novel regulator, 3β-sulfate-5-cholestenoic acid, of lipid metabolism and inflammation.American journal of physiology. Endocrinology and metabolism · 2025
    Article
  2. Article
  3. Review
  4. Review
  5. Larsucosterol: endogenous epigenetic regulator for treating chronic and acute liver diseases.American journal of physiology. Endocrinology and metabolism · 2024
    Review
  6. Cholestenoic acid as endogenous epigenetic regulator decreases hepatocyte lipid accumulation in vitro and in vivo.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  7. Human sulfotransferaseFrontiers in genetics · 2024
    Review
  8. 25-Hydroxycholesterol in health and diseases.Journal of lipid research · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. [Significance of lipidomics in liver fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Shunlin RenDepartments of Medicine, McGuire Veterans Affairs Medical Center/Virginia Commonwealth University, Richmond, Virginia.
Yanxia Ning
Hunter Holmes McGuire VA Medical Center · US

Funding

REGULATION OF CHOLESTEROL METABOLISMR01HL078898 · NHLBI · RICHMOND INSTITUTE FOR VETERANS RESEARCH · PI REN, SHUNLIN · 2006 to 2010
$1.5M
Novel Regulatory Pathway in Prevention of AtherosclerosisI01BX001874 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI REN, SHUNLIN · 2013 to 2016
–
BLRD VA I01 BX001874NHLBI NIH HHS R01 HL-078898NHLBI NIH HHS R01 HL078898
6 · The paper itself

Abstract

Intracellular lipid accumulation, inflammatory responses, and subsequent apoptosis are the major pathogenic events of metabolic disorders, including atherosclerosis and nonalcoholic fatty liver diseases. Recently, a novel regulatory oxysterol, 5-cholesten-3b, 25-diol 3-sulfate (25HC3S), has been identified, and hydroxysterol sulfotransferase 2B1b (SULT2B1b) has been elucidated as the key enzyme for its biosynthesis from 25-hydroxycholesterol (25HC) via oxysterol sulfation. The product 25HC3S and the substrate 25HC have been shown to coordinately regulate lipid metabolism, inflammatory responses, and cell proliferation in vitro and in vivo. 25HC3S decreases levels of the nuclear liver oxysterol receptor (LXR) and sterol regulatory element-binding proteins (SREBPs), inhibits SREBP processing, subsequently downregulates key enzymes in lipid biosynthesis, decreases intracellular lipid levels in hepatocytes and THP-1-derived macrophages, prevents apoptosis, and promotes cell proliferation in liver tissues. Furthermore, 25HC3S increases nuclear PPARγ and cytosolic IκBα and decreases nuclear NF-κB levels and proinflammatory cytokine expression and secretion when cells are challenged with LPS and TNFα. In contrast to 25HC3S, 25HC, a known LXR ligand, increases nuclear LXR and decreases nuclear PPARs and cytosol IκBα levels. In this review, we summarize our recent findings, including the discovery of the regulatory oxysterol sulfate, its biosynthetic pathway, and its functional mechanism. We also propose that oxysterol sulfation functions as a regulatory signaling pathway.

Indexed as

AnimalsCell ProliferationCholesterol EstersHumansHydroxycholesterolsInflammationLipid MetabolismLiver X ReceptorsOrphan Nuclear ReceptorsSterol Regulatory Element Binding ProteinsSulfatases25-hydroxycholesterol25-hydroxycholesterol 3-sulfateCholesterol EstersHydroxycholesterolsLiver X ReceptorsOrphan Nuclear ReceptorsSterol Regulatory Element Binding ProteinsSulfatases25HC3S, LXR, SREBPs, IκB, NF-κB, PPARscholesterol and triglyceride metabolismnuclear receptoroxysterol sulfate

Identifiers

PMID24302009
PMCPMC3920008
OpenAlexW2087709414

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.