Tryptophan Metabolism and COVID-19-Induced Skeletal Muscle Damage: Is ACE2 a Key Regulator?

The severity of coronavirus disease 2019 (COVID-19) is characterized by systemic damage to organs, including skeletal muscle, due to excessive secretion of inflammatory cytokines. Clinical studies have suggested that the kynurenine pathway of tryptophan metabolism is selectively enhanced in patients...

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Detalles Bibliográficos
Autores principales: Takeshita, Hikari, Yamamoto, Koichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Nutrition
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9028463/
https://www.ncbi.nlm.nih.gov/pubmed/35463998
http://dx.doi.org/10.3389/fnut.2022.868845
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author Takeshita, Hikari
Yamamoto, Koichi
author_facet Takeshita, Hikari
Yamamoto, Koichi
author_sort Takeshita, Hikari
collection PubMed
description The severity of coronavirus disease 2019 (COVID-19) is characterized by systemic damage to organs, including skeletal muscle, due to excessive secretion of inflammatory cytokines. Clinical studies have suggested that the kynurenine pathway of tryptophan metabolism is selectively enhanced in patients with severe COVID-19. In addition to acting as a receptor for severe acute respiratory syndrome coronavirus 2, the causative virus of COVID-19, angiotensin converting enzyme 2 (ACE2) contributes to tryptophan absorption and inhibition of the renin-angiotensin system. In this article, we review previous studies to assess the potential for a link between tryptophan metabolism, ACE2, and skeletal muscle damage in patients with COVID-19.
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spelling pubmed-90284632022-04-23 Tryptophan Metabolism and COVID-19-Induced Skeletal Muscle Damage: Is ACE2 a Key Regulator? Takeshita, Hikari Yamamoto, Koichi Front Nutr Nutrition The severity of coronavirus disease 2019 (COVID-19) is characterized by systemic damage to organs, including skeletal muscle, due to excessive secretion of inflammatory cytokines. Clinical studies have suggested that the kynurenine pathway of tryptophan metabolism is selectively enhanced in patients with severe COVID-19. In addition to acting as a receptor for severe acute respiratory syndrome coronavirus 2, the causative virus of COVID-19, angiotensin converting enzyme 2 (ACE2) contributes to tryptophan absorption and inhibition of the renin-angiotensin system. In this article, we review previous studies to assess the potential for a link between tryptophan metabolism, ACE2, and skeletal muscle damage in patients with COVID-19. Frontiers Media S.A. 2022-04-08 /pmc/articles/PMC9028463/ /pubmed/35463998 http://dx.doi.org/10.3389/fnut.2022.868845 Text en Copyright © 2022 Takeshita and Yamamoto. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Nutrition
Takeshita, Hikari
Yamamoto, Koichi
Tryptophan Metabolism and COVID-19-Induced Skeletal Muscle Damage: Is ACE2 a Key Regulator?
title Tryptophan Metabolism and COVID-19-Induced Skeletal Muscle Damage: Is ACE2 a Key Regulator?
title_full Tryptophan Metabolism and COVID-19-Induced Skeletal Muscle Damage: Is ACE2 a Key Regulator?
title_fullStr Tryptophan Metabolism and COVID-19-Induced Skeletal Muscle Damage: Is ACE2 a Key Regulator?
title_full_unstemmed Tryptophan Metabolism and COVID-19-Induced Skeletal Muscle Damage: Is ACE2 a Key Regulator?
title_short Tryptophan Metabolism and COVID-19-Induced Skeletal Muscle Damage: Is ACE2 a Key Regulator?
title_sort tryptophan metabolism and covid-19-induced skeletal muscle damage: is ace2 a key regulator?
topic Nutrition
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9028463/
https://www.ncbi.nlm.nih.gov/pubmed/35463998
http://dx.doi.org/10.3389/fnut.2022.868845
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