SARS-CoV-2 Nsp6 damages Drosophila heart and mouse cardiomyocytes through MGA/MAX complex-mediated increased glycolysis

SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The presence of virus in cardiac tissue of patients with COVID-19 suggests this is a direct, rather than secondary, effect of infection. Here, by expres...

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Published inCommunications biology Vol. 5; no. 1; pp. 1 - 15
Main Authors Zhu, Jun-yi, Wang, Guanglei, Huang, Xiaohu, Lee, Hangnoh, Lee, Jin-Gu, Yang, Penghua, van de Leemput, Joyce, Huang, Weiliang, Kane, Maureen A., Yang, Peixin, Han, Zhe
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 30.09.2022
Nature Publishing Group
Nature Portfolio
Subjects
13/51
13/89
14/10
14/19
45/91
631/80/221
631/80/304
64/24
64/60
82/58
Biology
Biomedical and Life Sciences
Cardiomyocytes
Congestive heart failure
Coronaviruses
COVID-19
Drosophila
Glucose
Glycolysis
Heart failure
Insects
Life Sciences
Mitochondria
Myc protein
Pathology
Phenotypes
Reactive oxygen species
Respiratory diseases
Severe acute respiratory syndrome coronavirus 2
Transcriptomics
Viruses
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Abstract SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The presence of virus in cardiac tissue of patients with COVID-19 suggests this is a direct, rather than secondary, effect of infection. Here, by expressing individual SARS-CoV-2 proteins in the Drosophila heart, we demonstrate interaction of virus Nsp6 with host proteins of the MGA/MAX complex (MGA, PCGF6 and TFDP1). Complementing transcriptomic data from the fly heart reveal that this interaction blocks the antagonistic MGA/MAX complex, which shifts the balance towards MYC/MAX and activates glycolysis—with similar findings in mouse cardiomyocytes. Further, the Nsp6 -induced glycolysis disrupts cardiac mitochondrial function, known to increase reactive oxygen species (ROS) in heart failure; this could explain COVID-19-associated cardiac pathology. Inhibiting the glycolysis pathway by 2-deoxy-D-glucose (2DG) treatment attenuates the Nsp6 -induced cardiac phenotype in flies and mice. These findings point to glycolysis as a potential pharmacological target for treating COVID-19-associated heart failure. SARS-CoV-2 protein expression studies in the Drosophila heart suggest a cause of COVID-19-associated cardiac pathology via interaction of virus Nsp6 with the host MGA/MAX complex disrupting glycolysis and cardiac mitochondrial function.
AbstractList SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The presence of virus in cardiac tissue of patients with COVID-19 suggests this is a direct, rather than secondary, effect of infection. Here, by expressing individual SARS-CoV-2 proteins in the Drosophila heart, we demonstrate interaction of virus Nsp6 with host proteins of the MGA/MAX complex (MGA, PCGF6 and TFDP1). Complementing transcriptomic data from the fly heart reveal that this interaction blocks the antagonistic MGA/MAX complex, which shifts the balance towards MYC/MAX and activates glycolysis—with similar findings in mouse cardiomyocytes. Further, the Nsp6 -induced glycolysis disrupts cardiac mitochondrial function, known to increase reactive oxygen species (ROS) in heart failure; this could explain COVID-19-associated cardiac pathology. Inhibiting the glycolysis pathway by 2-deoxy-D-glucose (2DG) treatment attenuates the Nsp6 -induced cardiac phenotype in flies and mice. These findings point to glycolysis as a potential pharmacological target for treating COVID-19-associated heart failure. SARS-CoV-2 protein expression studies in the Drosophila heart suggest a cause of COVID-19-associated cardiac pathology via interaction of virus Nsp6 with the host MGA/MAX complex disrupting glycolysis and cardiac mitochondrial function.
SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The presence of virus in cardiac tissue of patients with COVID-19 suggests this is a direct, rather than secondary, effect of infection. Here, by expressing individual SARS-CoV-2 proteins in the Drosophila heart, we demonstrate interaction of virus Nsp6 with host proteins of the MGA/MAX complex (MGA, PCGF6 and TFDP1). Complementing transcriptomic data from the fly heart reveal that this interaction blocks the antagonistic MGA/MAX complex, which shifts the balance towards MYC/MAX and activates glycolysis—with similar findings in mouse cardiomyocytes. Further, the Nsp6-induced glycolysis disrupts cardiac mitochondrial function, known to increase reactive oxygen species (ROS) in heart failure; this could explain COVID-19-associated cardiac pathology. Inhibiting the glycolysis pathway by 2-deoxy-D-glucose (2DG) treatment attenuates the Nsp6-induced cardiac phenotype in flies and mice. These findings point to glycolysis as a potential pharmacological target for treating COVID-19-associated heart failure.SARS-CoV-2 protein expression studies in the Drosophila heart suggest a cause of COVID-19-associated cardiac pathology via interaction of virus Nsp6 with the host MGA/MAX complex disrupting glycolysis and cardiac mitochondrial function.
SARS-CoV-2 protein expression studies in the Drosophila heart suggest a cause of COVID-19-associated cardiac pathology via interaction of virus Nsp6 with the host MGA/MAX complex disrupting glycolysis and cardiac mitochondrial function.
Abstract SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The presence of virus in cardiac tissue of patients with COVID-19 suggests this is a direct, rather than secondary, effect of infection. Here, by expressing individual SARS-CoV-2 proteins in the Drosophila heart, we demonstrate interaction of virus Nsp6 with host proteins of the MGA/MAX complex (MGA, PCGF6 and TFDP1). Complementing transcriptomic data from the fly heart reveal that this interaction blocks the antagonistic MGA/MAX complex, which shifts the balance towards MYC/MAX and activates glycolysis—with similar findings in mouse cardiomyocytes. Further, the Nsp6 -induced glycolysis disrupts cardiac mitochondrial function, known to increase reactive oxygen species (ROS) in heart failure; this could explain COVID-19-associated cardiac pathology. Inhibiting the glycolysis pathway by 2-deoxy-D-glucose (2DG) treatment attenuates the Nsp6 -induced cardiac phenotype in flies and mice. These findings point to glycolysis as a potential pharmacological target for treating COVID-19-associated heart failure.
ArticleNumber 1039
Author Yang, Penghua
Lee, Jin-Gu
Wang, Guanglei
van de Leemput, Joyce
Huang, Xiaohu
Huang, Weiliang
Lee, Hangnoh
Han, Zhe
Zhu, Jun-yi
Kane, Maureen A.
Yang, Peixin
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  surname: Huang
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  surname: van de Leemput
  fullname: van de Leemput, Joyce
  organization: Center for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine
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  givenname: Weiliang
  surname: Huang
  fullname: Huang, Weiliang
  organization: Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, University of Queensland
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  orcidid: 0000-0002-2104-0699
  surname: Yang
  fullname: Yang, Peixin
  organization: Department of Obstetrics, Gynecology & Reproductive Sciences, University of Maryland School of Medicine
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  givenname: Zhe
  orcidid: 0000-0002-5177-7798
  surname: Han
  fullname: Han, Zhe
  email: zhan@som.umaryland.edu
  organization: Center for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine, Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine
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Snippet SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The...
Abstract SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes....
SARS-CoV-2 protein expression studies in the Drosophila heart suggest a cause of COVID-19-associated cardiac pathology via interaction of virus Nsp6 with the...
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Biology
Biomedical and Life Sciences
Cardiomyocytes
Congestive heart failure
Coronaviruses
COVID-19
Drosophila
Glucose
Glycolysis
Heart failure
Insects
Life Sciences
Mitochondria
Myc protein
Pathology
Phenotypes
Reactive oxygen species
Respiratory diseases
Severe acute respiratory syndrome coronavirus 2
Transcriptomics
Viruses
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Title SARS-CoV-2 Nsp6 damages Drosophila heart and mouse cardiomyocytes through MGA/MAX complex-mediated increased glycolysis
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