Evidence map›Paper›PMID 32416353›Full record

ArticleRedox biology2020

Relationship between PMN-endothelium interactions, ROS production and Beclin-1 in type 2 diabetes.

Aranzazu M De Marañon, Francesca Iannantuoni, Zaida Abad-Jiménez, Francisco Canet, Pedro Díaz-Pozo, Sandra López-Domènech, Ana Jover, Carlos Morillas, Guillermo Mariño, Nadezda Apostolova and 2 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

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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

12 authors at 4 institutions in 1 country.

Aranzazu M De MarañonService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Francesca IannantuoniService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Zaida Abad-JiménezService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Francisco CanetService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Pedro Díaz-PozoService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Sandra López-DomènechService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Ana JoverService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Carlos MorillasService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.
Guillermo MariñoInstituto de Investigación Sanitaria del Principado de Asturias, 33011, Oviedo, Spain.
Nadezda ApostolovaCIBERehd - Department of Pharmacology, University of Valencia, Valencia, Spain.
Milagros RochaService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; CIBERehd - Department of Pharmacology, University of Valencia, Valencia, Spain. Electronic address: milagros.rocha@uv.es.
Victor M VictorService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; CIBERehd - Department of Pharmacology, University of Valencia, Valencia, Spain; Department of Physiology, University of Valencia, Valencia, Spain. Electronic address: victor.victor@uv.es.
Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana · ESHospital Universitario Doctor Peset · ESInstituto de Investigación Sanitaria del Principado de Asturias · ESUniversitat de València · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes is closely related to oxidative stress and cardiovascular diseases. In this study, we hypothesized that polymorphonuclear leukocytes (PMN)-endothelium interactions and autophagy are associated. We evaluated PMN-endothelial interactions, ROS production and autophagy parameters in 47 type 2 diabetic patients and 57 control subjects. PMNs from type 2 diabetic patients exhibited slower rolling velocity (p < 0.001), higher rolling flux (p < 0.001) and adhesion (p < 0.001) in parallel to higher levels of total (p < 0.05) and mitochondrial ROS (p < 0.05). When the protein expression of autophagy markers was analysed, an increase of Beclin-1 (p < 0.05), LC3I (p < 0.05), LC3II (p < 0.01) and LC3II/LC3I ratio (p < 0.05) was observed. Several correlations between ROS and leukocyte-endothelium parameters were found. Interestingly, in control subjects, an increase of Beclin-1 levels was accompanied by a decrease in the number of rolling (r = 0.561) and adhering PMNs (r = 0.560) and a rise in the velocity of the rolling PMNs (r = 0.593). In contrast, in the type 2 diabetic population, a rise in Beclin-1 levels was related to an increase in the number of rolling (r = 0.437), and adhering PMNs (r = 0.467). These results support the hypothesis that PMN-endothelium interactions, ROS levels and formation of autophagosomes, especially Beclin-1 levels, are enhanced in type 2 diabetes.

Indexed as

Diabetes Mellitus, Type 2NeutrophilsAutophagyBeclin-1Case-Control StudiesCell AdhesionEndotheliumHumansReactive Oxygen SpeciesBeclin-1Reactive Oxygen SpeciesAutophagyMitochondriaOxidative stressPMN-Endothelium interactionsROSType 2 diabetes

Identifiers

PMID32416353
PMCPMC7226867
OpenAlexW3022648787

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.