Advanced-glycation end-products axis: a contributor to the risk of severe illness from COVID-19 in diabetes patients
Author
dc.contributor.author
Rojas, Armando
Author
dc.contributor.author
Lindner, Cristian
Author
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González, Ileana
Author
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Morales Segura, Miguel
Admission date
dc.date.accessioned
2021-10-14T12:54:44Z
Available date
dc.date.available
2021-10-14T12:54:44Z
Publication date
dc.date.issued
2021
Cita de ítem
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World J Diabetes 2021 May 15; 12(5): 590-602
es_ES
Identifier
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10.4239/wjd.v12.i5.590
Identifier
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https://repositorio.uchile.cl/handle/2250/182244
Abstract
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Compelling pieces of evidence derived from both clinical and experimental research has demonstrated the crucial role of the receptor for advanced-glycation end-products (RAGE) in orchestrating a plethora of proinflammatory cellular responses leading to many of the complications and end-organ damages reported in patients with diabetes mellitus (DM). During the coronavirus disease 2019 (COVID-19) pandemic, many clinical reports have pointed out that DM increases the risk of COVID-19 complications, hospitalization requirements, as well as the overall severe acute respiratory syndrome coronavirus 2 case-fatality rate. In the present review, we intend to focus on how the basal activation state of the RAGE axis in common preexisting conditions in DM patients such as endothelial dysfunction and hyperglycemia-related prothrombotic phenotype, as well as the contribution of RAGE signaling in lung inflammation, may then lead to the increased mortality risk of COVID-19 in these patients. Additionally, the crosstalk between the RAGE axis with either another severe acute respiratory syndrome coronavirus 2 receptor molecule different of angiotensin-converting enzyme 2 or the renin-angiotensin system imbalance produced by viral infection, as well as the role of this multi-ligand receptor on the obesity-associated low-grade inflammation in the higher risk for severe illness reported in diabetes patients with COVID-19, are also discussed.
es_ES
Lenguage
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en
es_ES
Publisher
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Baishideng Publishing Group, Estados Unidos
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Type of license
dc.rights
Attribution-NonCommercial-NoDerivs 3.0 United States