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The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus
Vascular complications are the leading cause of morbidity and mortality among patients with type 2 diabetes mellitus (T2DM). These vascular abnormalities result in a chronic hyperglycemic state, which influences many signaling molecular pathways that initially lead to increased oxidative stress, inc...
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/PMC9266892/ https://www.ncbi.nlm.nih.gov/pubmed/35805996 http://dx.doi.org/10.3390/ijms23136995 |
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author | Sanabria-de la Torre, Raquel García-Fontana, Cristina González-Salvatierra, Sheila Andújar-Vera, Francisco Martínez-Heredia, Luis García-Fontana, Beatriz Muñoz-Torres, Manuel |
author_facet | Sanabria-de la Torre, Raquel García-Fontana, Cristina González-Salvatierra, Sheila Andújar-Vera, Francisco Martínez-Heredia, Luis García-Fontana, Beatriz Muñoz-Torres, Manuel |
author_sort | Sanabria-de la Torre, Raquel |
collection | PubMed |
description | Vascular complications are the leading cause of morbidity and mortality among patients with type 2 diabetes mellitus (T2DM). These vascular abnormalities result in a chronic hyperglycemic state, which influences many signaling molecular pathways that initially lead to increased oxidative stress, increased inflammation, and endothelial dysfunction, leading to both microvascular and macrovascular complications. Endothelial dysfunction represents the initial stage in both types of vascular complications; it represents “mandatory damage” in the development of microvascular complications and only “introductory damage” in the development of macrovascular complications. Increasing scientific evidence has revealed an important role of the Wnt pathway in the pathophysiology of the vascular wall. It is well known that the Wnt pathway is altered in patients with T2DM. This review aims to be an update of the current literature related to the Wnt pathway molecules that are altered in patients with T2DM, which may also be the cause of damage to the vasculature. Both microvascular complications (retinopathy, nephropathy, and neuropathy) and macrovascular complications (coronary artery disease, cerebrovascular disease, and peripheral arterial disease) are analyzed. This review aims to concisely concentrate all the evidence to facilitate the view on the vascular involvement of the Wnt pathway and its components by highlighting the importance of exploring possible therapeutic strategy for patients with T2DM who develop vascular pathologies. |
format | Online Article Text |
id | pubmed-9266892 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-92668922022-07-09 The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus Sanabria-de la Torre, Raquel García-Fontana, Cristina González-Salvatierra, Sheila Andújar-Vera, Francisco Martínez-Heredia, Luis García-Fontana, Beatriz Muñoz-Torres, Manuel Int J Mol Sci Review Vascular complications are the leading cause of morbidity and mortality among patients with type 2 diabetes mellitus (T2DM). These vascular abnormalities result in a chronic hyperglycemic state, which influences many signaling molecular pathways that initially lead to increased oxidative stress, increased inflammation, and endothelial dysfunction, leading to both microvascular and macrovascular complications. Endothelial dysfunction represents the initial stage in both types of vascular complications; it represents “mandatory damage” in the development of microvascular complications and only “introductory damage” in the development of macrovascular complications. Increasing scientific evidence has revealed an important role of the Wnt pathway in the pathophysiology of the vascular wall. It is well known that the Wnt pathway is altered in patients with T2DM. This review aims to be an update of the current literature related to the Wnt pathway molecules that are altered in patients with T2DM, which may also be the cause of damage to the vasculature. Both microvascular complications (retinopathy, nephropathy, and neuropathy) and macrovascular complications (coronary artery disease, cerebrovascular disease, and peripheral arterial disease) are analyzed. This review aims to concisely concentrate all the evidence to facilitate the view on the vascular involvement of the Wnt pathway and its components by highlighting the importance of exploring possible therapeutic strategy for patients with T2DM who develop vascular pathologies. MDPI 2022-06-23 /pmc/articles/PMC9266892/ /pubmed/35805996 http://dx.doi.org/10.3390/ijms23136995 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 | Review Sanabria-de la Torre, Raquel García-Fontana, Cristina González-Salvatierra, Sheila Andújar-Vera, Francisco Martínez-Heredia, Luis García-Fontana, Beatriz Muñoz-Torres, Manuel The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus |
title | The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus |
title_full | The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus |
title_fullStr | The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus |
title_full_unstemmed | The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus |
title_short | The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus |
title_sort | contribution of wnt signaling to vascular complications in type 2 diabetes mellitus |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9266892/ https://www.ncbi.nlm.nih.gov/pubmed/35805996 http://dx.doi.org/10.3390/ijms23136995 |
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