Evidence map›Paper›PMID 27877101›Full record

ReviewFrontiers in neuroscience2016

From Molecules to the Clinic: Linking Schizophrenia and Metabolic Syndrome through Sphingolipids Metabolism.

Rolando I Castillo, Leonel E Rojo, Marcela Henriquez-Henriquez, Hernán Silva, Alejandro Maturana, María J Villar, Manuel Fuentes, Pablo A Gaspar

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

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  15. Lipid Signaling During Gamete Maturation.Frontiers in cell and developmental biology · 2022
    Review
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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

8 authors at 5 institutions in 2 countries.

Rolando I CastilloTranslational Psychiatry Laboratory, Clínica Psiquiátrica Universitaria, Hospital Clínico Universidad de Chile Santiago, Chile.
Leonel E RojoDepartamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile Santiago, Chile.
Marcela Henriquez-HenriquezDepartamento de Laboratorios Clínicos, Escuela de Medicina, Pontificia Universidad Católica de ChileSantiago, Chile; Department of Pediatrics, Institute of Human Nutrition, College of Physicians and Surgeons, Columbia UniversityNew York, NY, USA; Department of Pathology and Cell Biology, Columbia UniversityNew York, NY, USA.
Hernán SilvaTranslational Psychiatry Laboratory, Clínica Psiquiátrica Universitaria, Hospital Clínico Universidad de ChileSantiago, Chile; Facultad de Medicina, Biomedical Neuroscience Institute, Universidad de ChileSantiago, Chile.
Alejandro MaturanaTranslational Psychiatry Laboratory, Clínica Psiquiátrica Universitaria, Hospital Clínico Universidad de Chile Santiago, Chile.
María J VillarTranslational Psychiatry Laboratory, Clínica Psiquiátrica Universitaria, Hospital Clínico Universidad de Chile Santiago, Chile.
Manuel FuentesDepartamento de Psiquiatría, Clínica Alemana Santiago, Chile.
Pablo A GasparTranslational Psychiatry Laboratory, Clínica Psiquiátrica Universitaria, Hospital Clínico Universidad de ChileSantiago, Chile; Facultad de Medicina, Biomedical Neuroscience Institute, Universidad de ChileSantiago, Chile; Departamento de Psiquiatría, Clínica AlemanaSantiago, Chile.
Hospital Clínico de la Universidad de Chile · CLClínica Alemana · CLColumbia University · USUniversidad de Santiago de Chile · CLUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome (MS) is a prevalent and severe comorbidity observed in schizophrenia (SZ). The exact nature of this association is controversial and very often accredited to the effects of psychotropic medications and disease-induced life-style modifications, such as inactive lifestyle, poor dietary choices, and smoking. However, drug therapy and disease-induced lifestyle factors are likely not the only factors contributing to the observed converging nature of these conditions, since an increased prevalence of MS is also observed in first episode and drug-naïve psychosis populations. MS and SZ share common intrinsic susceptibility factors and etiopathogenic mechanisms, which may change the way we approach clinical management of SZ patients. Among the most relevant common pathogenic pathways of SZ and MS are alterations in the sphingolipids (SLs) metabolism and SLs homeostasis. SLs have important structural functions as they participate in the formation of membrane "lipid rafts." SLs also play physiological roles in cell differentiation, proliferation, and inflammatory processes, which might be part of MS/SZ common pathophysiological processes. In this article we review a plausible mechanism to explain the link between MS and SZ through a disruption in SL homeostasis. Additionally, we provide insights on how this hypothesis can lead to the developing of new diagnostic/therapeutic technologies for SZ patients.

Indexed as

metabolic syndromepsychosisschizophreniasphingolipids

Identifiers

PMID27877101
PMCPMC5100552
OpenAlexW2555261483

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.