Evidence map›Paper›PMID 25637183›Full record

ReviewApoptosis : an international journal on programmed cell death2015

Glycosphingolipids and cell death: one aim, many ways.

Carmen Garcia-Ruiz, Albert Morales, José C Fernández-Checa

Open access · greenAbstract readReview
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.2field-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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  8. Hypoxic Status in COPD and ARDS Patients: Impact on Lipid Signature.International journal of molecular sciences · 2025
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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 2 countries.

Carmen Garcia-RuizDepartment of Cell Death and Proliferation, Instituto Investigaciones Biomedicas de Barcelona, CSIC, Barcelona, Spain.
Albert Morales
José C Fernández-Checa
Centro de Investigación Biomédica en Red · ESInstitut d'Investigacions Biomèdiques de Barcelona · ES

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
NIAAA NIH HHS P50 AA011999NIAAA NIH HHS P50-AA-11999
6 · The paper itself

Abstract

Glycosphingolipids (GSLs) are a family of bioactive lipids that in addition to their role in the regulation of structural properties of membrane bilayers have emerged as crucial players in many biological processes and signal transduction pathways. Rather than being uniformly distributed within membrane bilayers, GSLs are localized in selective domains called lipid rafts where many signaling platforms operate. One of the most important functions of GSLs, particularly ceramide, is their ability to regulate cell death pathways and hence cell fate. This complex role is accomplished by the ability of GSLs to act in distinct subcellular strategic centers, such as mitochondria, endoplasmic reticulum (ER) or lysosomes to mediate apoptosis, ER stress, autophagy, lysosomal membrane permeabilization and necroptosis. Hence better understanding the role of GSLs in cell death may be of relevance for a number of pathological processes and diseases, including neurodegeneration, metabolic liver diseases and cancer.

Indexed as

ApoptosisAnimalsAutophagyEndoplasmic Reticulum StressGlycosphingolipidsHumansLysosomesMitochondriaSignal TransductionSphingomyelin PhosphodiesteraseGlycosphingolipidsSphingomyelin Phosphodiesterase

Identifiers

PMID25637183
PMCPMC4691703
OpenAlexW1966758841

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.