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Review
. 2022 Nov 10:13:1037467.
doi: 10.3389/fmicb.2022.1037467. eCollection 2022.

Molecular and cellular mechanisms involved in tissue-specific metabolic modulation by SARS-CoV-2

Alef Aragão Carneiro Dos Santos  1 , Luiz Eduardo Rodrigues  1 , Amanda Lins Alecrim-Zeza  1 , Liliane de Araújo Ferreira  1 , Caio Dos Santos Trettel  1 , Gabriela Mandú Gimenes  1 , Adelson Fernandes da Silva  1 , Celso Pereira Batista Sousa-Filho  1 , Tamires Duarte Afonso Serdan  1   2 , Adriana Cristina Levada-Pires  1 , Elaine Hatanaka  1 , Fernanda Teixeira Borges  1   3 , Marcelo Paes de Barros  1 , Maria Fernanda Cury-Boaventura  1 , Gisele Lopes Bertolini  4 , Priscila Cassolla  4 , Gabriel Nasri Marzuca-Nassr  5 , Kaio Fernando Vitzel  6 , Tania Cristina Pithon-Curi  1 , Laureane Nunes Masi  1 , Rui Curi  1   7 , Renata Gorjao  1 , Sandro Massao Hirabara  1
Affiliations
Review

Molecular and cellular mechanisms involved in tissue-specific metabolic modulation by SARS-CoV-2

Alef Aragão Carneiro Dos Santos et al. Front Microbiol. .

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.

Keywords: SARS-CoV-2; inflammation; metabolism; oxidative stress; renin-angiotensin-aldosterone system.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
SARS-CoV-2-induced metabolic disturbances in central nervous system. CNS, central nervous system.
Figure 2
Figure 2
SARS-CoV-2-induced metabolic disturbances in skeletal muscle. AT1R, angiotensin II type 1 receptor; FA, fatty acid; HIF-1α, hypoxia-inducible factor-1 alpha; RAAS, renin-angiotensin-aldosterone system; ROS, reactive oxygen species.
Figure 3
Figure 3
SARS-CoV-2-induced metabolic disturbances in kidneys. FA, fatty acid; HIF-1α, hypoxia-inducible factor-1 alpha; RAAS, renin-angiotensin-aldosterone system; ROS, reactive oxygen species.
Figure 4
Figure 4
SARS-CoV-2-induced metabolic disturbances in heart. ATP adenosine triphosphate; CRP, C-reactive protein; ETC, electron transport chain; FA, fatty acid.
Figure 5
Figure 5
SARS-CoV-2-induced metabolic disturbances in liver. ROS, reactive oxygen species.
Figure 6
Figure 6
SARS-CoV-2-induced metabolic disturbances in gastrointestinal system. LPS, lipopolysaccharide.
Figure 7
Figure 7
Key points of the effects of SARS-CoV-2 on cell metabolism an tissue/organ dysfunction. ATP adenosine triphosphate; HIF-1α, hypoxia-inducible factor-1 alpha; RAAS, renin-angiotensin-aldosterone system; ROS, reactive oxygen species.
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