Evidence map›Paper›PMID 29778532›Full record

ReviewBiochemical and biophysical research communications2018

Non-alcoholic fatty liver disease: Insights from sphingolipidomics.

David J Montefusco, Jeremy C Allegood, Sarah Spiegel, L Ashley Cowart

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical and biophysical research communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Macrophage Plg-RJournal of thrombosis and haemostasis : JTH · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Assessing potential liver injury induced byPharmaceutical biology · 2022
    Article
  12. Article
  13. Article
  14. Analysis of the Sphingolipidome in NAFLD.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  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

4 authors at 1 institution in 1 country.

David J MontefuscoDepartment of Biochemistry and Molecular Biology and the Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.
Jeremy C AllegoodDepartment of Biochemistry and Molecular Biology and the Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.
Sarah SpiegelDepartment of Biochemistry and Molecular Biology and the Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.
L Ashley CowartDepartment of Biochemistry and Molecular Biology and the Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA; Hunter Holmes McGuire Veteran's Affairs Medical Center, Richmond, VA, USA. Electronic address: lauren.cowart@vcuhealth.org.
Virginia Commonwealth University · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Renato Martins · 1985 to 2026
$51.0M
SPHINGOSINE AS A MODULATOR OF CELLULAR PROLIFERATIONR01GM043880 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 1990 to 2023
$3.8M
Sphingolipids in Diabetic CardiomyopathyR01HL117233 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI COWART, LAUREN ASHLEY · 2014 to 2018
$1.9M
Sphingolipids in the Pathophysiology of Obesity and DiabetesI01BX000200 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI COWART, LAUREN ASHLEY · 2009 to 2025
–
BLRD VA I01 BX000200NCI NIH HHS P30 CA016059NHLBI NIH HHS R01 HL117233NIGMS NIH HHS R01 GM043880
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a major clinical concern and its treatment consumes abundant resources. While accumulation of lipids in hepatocytes initiates the disease, this in itself is not necessarily harmful; rather, initiation of inflammation and subsequent fibrosis and cirrhosis are critical steps in NAFLD pathology. Mechanisms linking lipid overload to downstream disease progression are not fully understood; however, bioactive lipid metabolism may underlie instigation of proinflammatory signaling. With the advent of high-throughput, sensitive, and quantitative mass spectrometry-based methods for assessing lipid profiles in NAFLD, several trends have emerged, including that increases in specific sphingolipids correlate with the transition from the relatively benign condition of simple fatty liver to the much more concerning inflamed state. Continued studies that implement sphingolipid profiling will enable the extrapolations of candidate enzymes and pathways involved in NAFLD, either in biopsies or plasma from human samples, and also in animal models, from which data are much more abundant. While most data thus far are derived from targeted lipidomics approaches, unbiased, semi-quantitative approaches hold additional promise for furthering our understanding of sphingolipids as markers of and players in NAFLD.

Indexed as

Lipid MetabolismMetabolic Networks and PathwaysAnimalsDisease ProgressionHumansLiverMolecular StructureNon-alcoholic Fatty Liver DiseaseSphingolipidsSphingolipidsCeramideLipidLipidomicsMetabolic syndromeNAFLDNASHNon-alcoholic fatty liver diseaseSphingolipidsSphingosine-1-phosphate

Identifiers

PMID29778532
PMCPMC6175671
OpenAlexW2803152100

What OpenQuestion holds

Textmetadata
LicenceTDM
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.