Evidence map›Paper›PMID 33645625›Full record

ArticleHistology and histopathology2021

Defective expression of the peroxisome regulators PPARα receptors and lysogenesis with increased cellular senescence in the venous wall of chronic venous disorder.

Miguel A Ortega, Oscar Fraile-Martínez, Leonel Pekarek, Miguel A Alvarez-Mon, Ángel Asúnsolo, Lara Sanchez-Trujillo, Santiago Coca, Julia Buján, Melchor Álvarez-Mon, Natalio García-Honduvilla and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Histology and histopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 12 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

11 authors at 4 institutions in 1 country.

Miguel A Ortega *Department of Medicine and Medical Specialities, Unit of Histology and Pathology, Faculty of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Oscar Fraile-Martínez *Department of Medicine and Medical Specialities, Unit of Histology and Pathology, Faculty of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Leonel Pekarek *Department of Medicine and Medical Specialities, Unit of Histology and Pathology, Faculty of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Miguel A Alvarez-MonDepartment of Medicine and Medical Specialities, Unit of Histology and Pathology, Faculty of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Ángel AsúnsoloRamón y Cajal Institute of Sanitary Research (IRYCIS), Madrid, Spain.
Lara Sanchez-TrujilloDepartment of Medicine and Medical Specialities, Unit of Histology and Pathology, Faculty of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Santiago CocaDepartment of Medicine and Medical Specialities, Unit of Histology and Pathology, Faculty of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Julia BujánRamón y Cajal Institute of Sanitary Research (IRYCIS), Madrid, Spain.
Melchor Álvarez-MonDepartment of Medicine and Medical Specialities, Unit of Histology and Pathology, Faculty of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Natalio García-Honduvilla *Department of Medicine and Medical Specialities, Unit of Histology and Pathology, Faculty of Medicine and Health Sciences, University of Alcalá, Alcalá de Henares, Madrid, Spain.
Felipe Sainz *Ramón y Cajal Institute of Sanitary Research (IRYCIS), Madrid, Spain.
Instituto Cajal · ESInstituto Ramón y Cajal de Investigación Sanitaria · ESHospital Central de la Defensa Gómez Ulla · ESUniversidad de Alcalá · ES

Funding

Instituto de Salud Carlos III (Plan Estatal de I+D+i 2013-2016) FIS-PI18/00912MITIC-CM B2017/BMD-3804
6 · The paper itself

Abstract

The pathogenesis of chronic venous disorder (CVeD) remains partially understood. A marked wall remodeling has been shown with potential accelerated tissue senescence. We have investigated the expression of peroxisome proliferator-activated receptor (PPAR) isoforms transcription factor EB (TFEB) as regulatory molecules of cellular homeostasis and makers of peroxisomal and lysosomal biogenesis. We have also quantified p16 expression as a cellular senescence marker. In specimens of maior safena vein from 35 CVeD and 27 healthy venous controls (HV), we studied the expression of PPAR-α, PPAR-β/δ, PPAR-γ, TFEB and p16 by RT-qPCR and immunohistochemical techniques. We have demonstrated a reduced gene and protein expression of the PPAR-α and PPAR-β/δ isoform as well as that of TFEB in the venous wall of CVeD patients, suggesting an altered peroxisomal and lysosomal biogenesis associated with an increased cellular senescence shown by increased p16 expression.

Indexed as

AdultAgedBiomarkersCellular SenescenceChronic DiseaseCyclin-Dependent Kinase Inhibitor p16FemaleHumansLysosomesMaleMiddle AgedPeroxisomesPPAR alphaSaphenous VeinVeinsBiomarkersCyclin-Dependent Kinase Inhibitor p16PPAR alpha

Identifiers

PMID33645625
OpenAlexW3135549352

What Socratic holds

Textmetadata
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 Socratic graph.