Evidence map›Paper›PMID 30140974›Full record

ReviewMolecular neurobiology2019

The Cross-Talk Between Sphingolipids and Insulin-Like Growth Factor Signaling: Significance for Aging and Neurodegeneration.

Henryk Jęśko, Adam Stępień, Walter J Lukiw, Robert P Strosznajder

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.7field-weighted citation impact, top 6% 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, 80 citations in OpenAlex.

  1. Article
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  17. The lipidomes ofAging · 2023
    Article
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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

4 authors at 3 institutions in 2 countries.

Henryk JęśkoDepartment of Cellular Signalling, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Pawińskiego, 5, 02-106, Poland.
Adam StępieńCentral Clinical Hospital of the Ministry of National Defense, Department of Neurology, Military Institute of Medicine, Warsaw, Szaserów, 128, 04-141, Poland.
Walter J LukiwLSU Neuroscience Center and Departments of Neurology and Ophthalmology, Louisiana State University School of Medicine, New Orleans, USA.
Robert P StrosznajderLaboratory of Preclinical Research and Environmental Agents, Department of Neurosurgery, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Pawińskiego, 5, 02-106, Poland. rstrosznajder@imdik.pan.pl.ORCID http://orcid.org/0000-0002-1922-0295
Mossakowski Medical Research Institute, Polish Academy of Sciences · PLCentral Clinical Hospital · PLLouisiana State University Health Sciences Center New Orleans · US

Funding

Narodowe Centrum Nauki NCN 2014/15/B/NZ3/01049
6 · The paper itself

Abstract

Bioactive sphingolipids: sphingosine, sphingosine-1-phosphate (S1P), ceramide, and ceramide-1-phosphate (C1P) are increasingly implicated in cell survival, proliferation, differentiation, and in multiple aspects of stress response in the nervous system. The opposite roles of closely related sphingolipid species in cell survival/death signaling is reflected in the concept of tightly controlled sphingolipid rheostat. Aging has a complex influence on sphingolipid metabolism, disturbing signaling pathways and the properties of lipid membranes. A metabolic signature of stress resistance-associated sphingolipids correlates with longevity in humans. Moreover, accumulating evidence suggests extensive links between sphingolipid signaling and the insulin-like growth factor I (IGF-I)-Akt-mTOR pathway (IIS), which is involved in the modulation of aging process and longevity. IIS integrates a wide array of metabolic signals, cross-talks with p53, nuclear factor κB (NF-κB), or reactive oxygen species (ROS) and influences gene expression to shape the cellular metabolic profile and stress resistance. The multiple connections between sphingolipids and IIS signaling suggest possible engagement of these compounds in the aging process itself, which creates a vulnerable background for the majority of neurodegenerative disorders.

Indexed as

Signal TransductionAgingAnimalsCellular SenescenceHumansNerve DegenerationSomatomedinsSphingolipidsSomatomedinsSphingolipidsAgingCeramideInsulin-like growth factorMitochondriaNeurodegenerationSphingosine-1-phosphate

Identifiers

PMID30140974
PMCPMC6476865
OpenAlexW2888531539

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.