Author:
Santos Alef Aragão Carneiro dos,Rodrigues Luiz Eduardo,Alecrim-Zeza Amanda Lins,de Araújo Ferreira Liliane,Trettel Caio dos Santos,Gimenes Gabriela Mandú,Silva Adelson Fernandes da,Sousa-Filho Celso Pereira Batista,Serdan Tamires Duarte Afonso,Levada-Pires Adriana Cristina,Hatanaka Elaine,Borges Fernanda Teixeira,de Barros Marcelo Paes,Cury-Boaventura Maria Fernanda,Bertolini Gisele Lopes,Cassolla Priscila,Marzuca-Nassr Gabriel Nasri,Vitzel Kaio Fernando,Pithon-Curi Tania Cristina,Masi Laureane Nunes,Curi Rui,Gorjao Renata,Hirabara Sandro Massao
Abstract
Coronavirus disease 2019 (COVID-19) is triggered by the SARS-CoV-2, which is able to infect and cause dysfunction not only in lungs, but also in multiple organs, including central nervous system, skeletal muscle, kidneys, heart, liver, and intestine. Several metabolic disturbances are associated with cell damage or tissue injury, but the mechanisms involved are not yet fully elucidated. Some potential mechanisms involved in the COVID-19-induced tissue dysfunction are proposed, such as: (a) High expression and levels of proinflammatory cytokines, including TNF-α IL-6, IL-1β, INF-α and INF-β, increasing the systemic and tissue inflammatory state; (b) Induction of oxidative stress due to redox imbalance, resulting in cell injury or death induced by elevated production of reactive oxygen species; and (c) Deregulation of the renin-angiotensin-aldosterone system, exacerbating the inflammatory and oxidative stress responses. In this review, we discuss the main metabolic disturbances observed in different target tissues of SARS-CoV-2 and the potential mechanisms involved in these changes associated with the tissue dysfunction.
Funder
São Paulo Research Foundation
Coordination for the Improvement of Higher Education Personnel
National Council for Scientific and Technological Development
Subject
Microbiology (medical),Microbiology
Cited by
4 articles.
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