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Venous Wall of Patients with Chronic Venous Disease Exhibits a Glycolytic Phenotype
Chronic venous disease (CVeD) is a rising medical condition characterized by a broad spectrum of disorders in the venous system. Varicose veins (VVs) represent a frequent clinical manifestation of CVeD, particularly in the lower limbs. Prior histopathological studies have defined a set of alteration...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9604927/ https://www.ncbi.nlm.nih.gov/pubmed/36294781 http://dx.doi.org/10.3390/jpm12101642 |
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author | Fraile-Martinez, Oscar García-Montero, Cielo Alvarez-Mon, Miguel Ángel Gomez-Lahoz, Ana M. Monserrat, Jorge Llavero-Valero, Maria Ruiz-Grande, Fernando Coca, Santiago Alvarez-Mon, Melchor Buján, Julia García-Honduvilla, Natalio Saz, Jose V. Ortega, Miguel A. |
author_facet | Fraile-Martinez, Oscar García-Montero, Cielo Alvarez-Mon, Miguel Ángel Gomez-Lahoz, Ana M. Monserrat, Jorge Llavero-Valero, Maria Ruiz-Grande, Fernando Coca, Santiago Alvarez-Mon, Melchor Buján, Julia García-Honduvilla, Natalio Saz, Jose V. Ortega, Miguel A. |
author_sort | Fraile-Martinez, Oscar |
collection | PubMed |
description | Chronic venous disease (CVeD) is a rising medical condition characterized by a broad spectrum of disorders in the venous system. Varicose veins (VVs) represent a frequent clinical manifestation of CVeD, particularly in the lower limbs. Prior histopathological studies have defined a set of alterations observed in the venous wall of patients with VVs, affecting their structure and behavior. Metabolic changes in the veins appear to be a critical biological mechanism aiding our understanding of the pathogenesis of CVeD. In this sense, previous studies have identified a potential role of a glycolytic phenotype in the development of different vascular disorders; however, its precise role in CVeD remains to be fully explored. Thus, the aim of the present study was to analyze the gene and protein expression of glucose transporter 1 (GLUT-1) and the glycolytic enzymes PGK-1, ALD, GA3PDH and LDH in the VVs of patients with CVeD (n = 35) in comparison to those expressed in healthy subjects. Our results display enhanced gene and protein expression of GLUT-1, PGK-1, ALD, GA3PDH and LDH in patients with CVeD, suggesting a glycolytic switch of the venous tissue. Greater understanding of the impact of this glycolytic switch in patients with CVeD is required to define a possible pathophysiological role or therapeutic implications of these changes. |
format | Online Article Text |
id | pubmed-9604927 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-96049272022-10-27 Venous Wall of Patients with Chronic Venous Disease Exhibits a Glycolytic Phenotype Fraile-Martinez, Oscar García-Montero, Cielo Alvarez-Mon, Miguel Ángel Gomez-Lahoz, Ana M. Monserrat, Jorge Llavero-Valero, Maria Ruiz-Grande, Fernando Coca, Santiago Alvarez-Mon, Melchor Buján, Julia García-Honduvilla, Natalio Saz, Jose V. Ortega, Miguel A. J Pers Med Article Chronic venous disease (CVeD) is a rising medical condition characterized by a broad spectrum of disorders in the venous system. Varicose veins (VVs) represent a frequent clinical manifestation of CVeD, particularly in the lower limbs. Prior histopathological studies have defined a set of alterations observed in the venous wall of patients with VVs, affecting their structure and behavior. Metabolic changes in the veins appear to be a critical biological mechanism aiding our understanding of the pathogenesis of CVeD. In this sense, previous studies have identified a potential role of a glycolytic phenotype in the development of different vascular disorders; however, its precise role in CVeD remains to be fully explored. Thus, the aim of the present study was to analyze the gene and protein expression of glucose transporter 1 (GLUT-1) and the glycolytic enzymes PGK-1, ALD, GA3PDH and LDH in the VVs of patients with CVeD (n = 35) in comparison to those expressed in healthy subjects. Our results display enhanced gene and protein expression of GLUT-1, PGK-1, ALD, GA3PDH and LDH in patients with CVeD, suggesting a glycolytic switch of the venous tissue. Greater understanding of the impact of this glycolytic switch in patients with CVeD is required to define a possible pathophysiological role or therapeutic implications of these changes. MDPI 2022-10-03 /pmc/articles/PMC9604927/ /pubmed/36294781 http://dx.doi.org/10.3390/jpm12101642 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Fraile-Martinez, Oscar García-Montero, Cielo Alvarez-Mon, Miguel Ángel Gomez-Lahoz, Ana M. Monserrat, Jorge Llavero-Valero, Maria Ruiz-Grande, Fernando Coca, Santiago Alvarez-Mon, Melchor Buján, Julia García-Honduvilla, Natalio Saz, Jose V. Ortega, Miguel A. Venous Wall of Patients with Chronic Venous Disease Exhibits a Glycolytic Phenotype |
title | Venous Wall of Patients with Chronic Venous Disease Exhibits a Glycolytic Phenotype |
title_full | Venous Wall of Patients with Chronic Venous Disease Exhibits a Glycolytic Phenotype |
title_fullStr | Venous Wall of Patients with Chronic Venous Disease Exhibits a Glycolytic Phenotype |
title_full_unstemmed | Venous Wall of Patients with Chronic Venous Disease Exhibits a Glycolytic Phenotype |
title_short | Venous Wall of Patients with Chronic Venous Disease Exhibits a Glycolytic Phenotype |
title_sort | venous wall of patients with chronic venous disease exhibits a glycolytic phenotype |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9604927/ https://www.ncbi.nlm.nih.gov/pubmed/36294781 http://dx.doi.org/10.3390/jpm12101642 |
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