Evidence map›Paper›PMID 28659813›Full record

ArticleFrontiers in physiology2017

Human Peritoneal Mesothelial Cell Death Induced by High-Glucose Hypertonic Solution Involves Ca

Felipe Simon, Pablo Tapia, Ricardo Armisen, Cesar Echeverria, Sebastian Gatica, Alejandro Vallejos, Alejandro Pacheco, Maria E Sanhueza, Miriam Alvo, Erico Segovia and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  3. TLR4 induced TRPM2 mediated neuropathic pain.Frontiers in pharmacology · 2024
    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

11 authors at 4 institutions in 1 country.

Felipe SimonDepartamento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad de Medicina, Universidad Andres BelloSantiago, Chile.
Pablo TapiaUnidad de Paciente Critico, Hospital Clínico Metropolitano de La FloridaSantiago, Chile.
Ricardo ArmisenCentro de Investigación y Tratamiento del Cancer, Facultad de Medicina, Universidad de ChileSantiago, Chile.
Cesar EcheverriaCentro Integrativo de Biología y Química Aplicada, Universidad Bernardo OHigginsSantiago, Chile.
Sebastian GaticaDepartamento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad de Medicina, Universidad Andres BelloSantiago, Chile.
Alejandro VallejosDepartamento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad de Medicina, Universidad Andres BelloSantiago, Chile.
Alejandro PachecoSección de Nefrología, Departamento de Medicina, Hospital Clínico Universidad de ChileSantiago, Chile.
Maria E SanhuezaSección de Nefrología, Departamento de Medicina, Hospital Clínico Universidad de ChileSantiago, Chile.
Miriam AlvoSección de Nefrología, Departamento de Medicina, Hospital Clínico Universidad de ChileSantiago, Chile.
Erico SegoviaCentro Integrativo de Biología y Química Aplicada, Universidad Bernardo OHigginsSantiago, Chile.
Rubén TorresSección de Nefrología, Departamento de Medicina, Hospital Clínico Universidad de ChileSantiago, Chile.
Hospital Clínico de la Universidad de Chile · CLUniversidad Andrés Bello · CLUniversidad Bernardo O'Higgins · CLUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic peritoneal dialysis (PD) therapy is equally efficient as hemodialysis while providing greater patient comfort and mobility. Therefore, PD is the treatment of choice for several types of renal patients. During PD, a high-glucose hyperosmotic (HGH) solution is administered into the peritoneal cavity to generate an osmotic gradient that promotes water and solutes transport from peritoneal blood to the dialysis solution. Unfortunately, PD has been associated with a loss of peritoneal viability and function through the generation of a severe inflammatory state that induces human peritoneal mesothelial cell (HPMC) death. Despite this deleterious effect, the precise molecular mechanism of HPMC death as induced by HGH solutions is far from being understood. Therefore, the aim of this study was to explore the pathways involved in HGH solution-induced HPMC death. HGH-induced HPMC death included influxes of intracellular Ca

Indexed as

cell deathdialysishypertonicitymesothelial cellperitoneal tissue

Identifiers

PMID28659813
PMCPMC5468383
OpenAlexW2625349179

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.