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Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2
Aging and pre-existing conditions in older patients increase severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) severity and its complications, although the causes remain unclear. Apart from acute pulmonary syndrome, Coronavirus 2019 (COVID-19) can increasingly induce chronic conditions. I...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Ltd.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7997138/ https://www.ncbi.nlm.nih.gov/pubmed/33775925 http://dx.doi.org/10.1016/j.drudis.2021.03.013 |
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author | Ho, Gilbert Ali, Alysha Takamatsu, Yoshiki Wada, Ryoko Masliah, Eliezer Hashimoto, Makoto |
author_facet | Ho, Gilbert Ali, Alysha Takamatsu, Yoshiki Wada, Ryoko Masliah, Eliezer Hashimoto, Makoto |
author_sort | Ho, Gilbert |
collection | PubMed |
description | Aging and pre-existing conditions in older patients increase severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) severity and its complications, although the causes remain unclear. Apart from acute pulmonary syndrome, Coronavirus 2019 (COVID-19) can increasingly induce chronic conditions. Importantly, SARS-CoV-2 triggers de novo type 2 diabetes mellitus (T2DM) linked to age-associated cardiovascular disease (CVD), cancers, and neurodegeneration. Mechanistically, SARS-CoV-2 induces inflammation, possibly through damage-associated molecular pattern (DAMP) signaling and ‘cytokine storm,’ causing insulin resistance and the adiponectin (APN) paradox, a phenomenon linking metabolic dysfunction to chronic disease. Accordingly, preventing the APN paradox by suppressing APN-related inflammatory signaling might prove beneficial. A better understanding could uncover novel therapies for SARS-CoV-2 and its chronic disorders. |
format | Online Article Text |
id | pubmed-7997138 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Elsevier Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-79971382021-03-29 Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2 Ho, Gilbert Ali, Alysha Takamatsu, Yoshiki Wada, Ryoko Masliah, Eliezer Hashimoto, Makoto Drug Discov Today Post-Screen (Grey) Aging and pre-existing conditions in older patients increase severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) severity and its complications, although the causes remain unclear. Apart from acute pulmonary syndrome, Coronavirus 2019 (COVID-19) can increasingly induce chronic conditions. Importantly, SARS-CoV-2 triggers de novo type 2 diabetes mellitus (T2DM) linked to age-associated cardiovascular disease (CVD), cancers, and neurodegeneration. Mechanistically, SARS-CoV-2 induces inflammation, possibly through damage-associated molecular pattern (DAMP) signaling and ‘cytokine storm,’ causing insulin resistance and the adiponectin (APN) paradox, a phenomenon linking metabolic dysfunction to chronic disease. Accordingly, preventing the APN paradox by suppressing APN-related inflammatory signaling might prove beneficial. A better understanding could uncover novel therapies for SARS-CoV-2 and its chronic disorders. Elsevier Ltd. 2021-08 2021-03-26 /pmc/articles/PMC7997138/ /pubmed/33775925 http://dx.doi.org/10.1016/j.drudis.2021.03.013 Text en © 2021 Elsevier Ltd. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Post-Screen (Grey) Ho, Gilbert Ali, Alysha Takamatsu, Yoshiki Wada, Ryoko Masliah, Eliezer Hashimoto, Makoto Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2 |
title | Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2 |
title_full | Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2 |
title_fullStr | Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2 |
title_full_unstemmed | Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2 |
title_short | Diabetes, inflammation, and the adiponectin paradox: Therapeutic targets in SARS-CoV-2 |
title_sort | diabetes, inflammation, and the adiponectin paradox: therapeutic targets in sars-cov-2 |
topic | Post-Screen (Grey) |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7997138/ https://www.ncbi.nlm.nih.gov/pubmed/33775925 http://dx.doi.org/10.1016/j.drudis.2021.03.013 |
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