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SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress

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SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress. / Tangos, Melina; Budde, Heidi; Kolijn, Detmar; Sieme, Marcel; Zhazykbayeva, Saltanat; Lódi, Mária; Herwig, Melissa; Gömöri, Kamilla; Hassoun, Roua; Robinson, Emma Louise; Meister, Toni Luise; Jaquet, Kornelia; Kovács, Árpád; Mustroph, Julian; Evert, Katja; Babel, Nina; Fagyas, Miklós; Lindner, Diana; Püschel, Klaus; Westermann, Dirk; Mannherz, Hans Georg; Paneni, Francesco; Pfaender, Stephanie; Tóth, Attila; Mügge, Andreas; Sossalla, Samuel; Hamdani, Nazha.

in: INT J CARDIOL, Jahrgang 362, 01.09.2022, S. 196-205.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Tangos, M, Budde, H, Kolijn, D, Sieme, M, Zhazykbayeva, S, Lódi, M, Herwig, M, Gömöri, K, Hassoun, R, Robinson, EL, Meister, TL, Jaquet, K, Kovács, Á, Mustroph, J, Evert, K, Babel, N, Fagyas, M, Lindner, D, Püschel, K, Westermann, D, Mannherz, HG, Paneni, F, Pfaender, S, Tóth, A, Mügge, A, Sossalla, S & Hamdani, N 2022, 'SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress', INT J CARDIOL, Jg. 362, S. 196-205. https://doi.org/10.1016/j.ijcard.2022.05.055

APA

Tangos, M., Budde, H., Kolijn, D., Sieme, M., Zhazykbayeva, S., Lódi, M., Herwig, M., Gömöri, K., Hassoun, R., Robinson, E. L., Meister, T. L., Jaquet, K., Kovács, Á., Mustroph, J., Evert, K., Babel, N., Fagyas, M., Lindner, D., Püschel, K., ... Hamdani, N. (2022). SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress. INT J CARDIOL, 362, 196-205. https://doi.org/10.1016/j.ijcard.2022.05.055

Vancouver

Tangos M, Budde H, Kolijn D, Sieme M, Zhazykbayeva S, Lódi M et al. SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress. INT J CARDIOL. 2022 Sep 1;362:196-205. https://doi.org/10.1016/j.ijcard.2022.05.055

Bibtex

@article{fe579ce19c874063b1a3c09a80665796,
title = "SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress",
abstract = "INTRODUCTION: The respiratory illness triggered by severe acute respiratory syndrome virus-2 (SARS-CoV-2) is often particularly serious or fatal amongst patients with pre-existing heart conditions. Although the mechanisms underlying SARS-CoV-2-related cardiac damage remain elusive, inflammation (i.e. 'cytokine storm') and oxidative stress are likely involved.METHODS AND RESULTS: Here we sought to determine: 1) if cardiomyocytes are targeted by SARS-CoV-2 and 2) how inflammation and oxidative stress promote the viral entry into cardiac cells. We analysed pro-inflammatory and oxidative stress and its impact on virus entry and virus-associated cardiac damage from SARS-CoV-2 infected patients and compared it to left ventricular myocardial tissues obtained from non-infected transplanted hearts either from end stage heart failure or non-failing hearts (donor group). We found that neuropilin-1 potentiates SARS-CoV-2 entry into human cardiomyocytes, a phenomenon driven by inflammatory and oxidant signals. These changes accounted for increased proteases activity and apoptotic markers thus leading to cell damage and apoptosis.CONCLUSION: This study provides new insights into the mechanisms of SARS-CoV-2 entry into the heart and defines promising targets for antiviral interventions for COVID-19 patients with pre-existing heart conditions or patients with co-morbidities.",
keywords = "COVID-19, Humans, Inflammation, Myocytes, Cardiac, Oxidative Stress, SARS-CoV-2",
author = "Melina Tangos and Heidi Budde and Detmar Kolijn and Marcel Sieme and Saltanat Zhazykbayeva and M{\'a}ria L{\'o}di and Melissa Herwig and Kamilla G{\"o}m{\"o}ri and Roua Hassoun and Robinson, {Emma Louise} and Meister, {Toni Luise} and Kornelia Jaquet and {\'A}rp{\'a}d Kov{\'a}cs and Julian Mustroph and Katja Evert and Nina Babel and Mikl{\'o}s Fagyas and Diana Lindner and Klaus P{\"u}schel and Dirk Westermann and Mannherz, {Hans Georg} and Francesco Paneni and Stephanie Pfaender and Attila T{\'o}th and Andreas M{\"u}gge and Samuel Sossalla and Nazha Hamdani",
note = "Copyright {\textcopyright} 2022 The Author(s). Published by Elsevier B.V. All rights reserved.",
year = "2022",
month = sep,
day = "1",
doi = "10.1016/j.ijcard.2022.05.055",
language = "English",
volume = "362",
pages = "196--205",
journal = "INT J CARDIOL",
issn = "0167-5273",
publisher = "Elsevier Ireland Ltd",

}

RIS

TY - JOUR

T1 - SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress

AU - Tangos, Melina

AU - Budde, Heidi

AU - Kolijn, Detmar

AU - Sieme, Marcel

AU - Zhazykbayeva, Saltanat

AU - Lódi, Mária

AU - Herwig, Melissa

AU - Gömöri, Kamilla

AU - Hassoun, Roua

AU - Robinson, Emma Louise

AU - Meister, Toni Luise

AU - Jaquet, Kornelia

AU - Kovács, Árpád

AU - Mustroph, Julian

AU - Evert, Katja

AU - Babel, Nina

AU - Fagyas, Miklós

AU - Lindner, Diana

AU - Püschel, Klaus

AU - Westermann, Dirk

AU - Mannherz, Hans Georg

AU - Paneni, Francesco

AU - Pfaender, Stephanie

AU - Tóth, Attila

AU - Mügge, Andreas

AU - Sossalla, Samuel

AU - Hamdani, Nazha

N1 - Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.

PY - 2022/9/1

Y1 - 2022/9/1

N2 - INTRODUCTION: The respiratory illness triggered by severe acute respiratory syndrome virus-2 (SARS-CoV-2) is often particularly serious or fatal amongst patients with pre-existing heart conditions. Although the mechanisms underlying SARS-CoV-2-related cardiac damage remain elusive, inflammation (i.e. 'cytokine storm') and oxidative stress are likely involved.METHODS AND RESULTS: Here we sought to determine: 1) if cardiomyocytes are targeted by SARS-CoV-2 and 2) how inflammation and oxidative stress promote the viral entry into cardiac cells. We analysed pro-inflammatory and oxidative stress and its impact on virus entry and virus-associated cardiac damage from SARS-CoV-2 infected patients and compared it to left ventricular myocardial tissues obtained from non-infected transplanted hearts either from end stage heart failure or non-failing hearts (donor group). We found that neuropilin-1 potentiates SARS-CoV-2 entry into human cardiomyocytes, a phenomenon driven by inflammatory and oxidant signals. These changes accounted for increased proteases activity and apoptotic markers thus leading to cell damage and apoptosis.CONCLUSION: This study provides new insights into the mechanisms of SARS-CoV-2 entry into the heart and defines promising targets for antiviral interventions for COVID-19 patients with pre-existing heart conditions or patients with co-morbidities.

AB - INTRODUCTION: The respiratory illness triggered by severe acute respiratory syndrome virus-2 (SARS-CoV-2) is often particularly serious or fatal amongst patients with pre-existing heart conditions. Although the mechanisms underlying SARS-CoV-2-related cardiac damage remain elusive, inflammation (i.e. 'cytokine storm') and oxidative stress are likely involved.METHODS AND RESULTS: Here we sought to determine: 1) if cardiomyocytes are targeted by SARS-CoV-2 and 2) how inflammation and oxidative stress promote the viral entry into cardiac cells. We analysed pro-inflammatory and oxidative stress and its impact on virus entry and virus-associated cardiac damage from SARS-CoV-2 infected patients and compared it to left ventricular myocardial tissues obtained from non-infected transplanted hearts either from end stage heart failure or non-failing hearts (donor group). We found that neuropilin-1 potentiates SARS-CoV-2 entry into human cardiomyocytes, a phenomenon driven by inflammatory and oxidant signals. These changes accounted for increased proteases activity and apoptotic markers thus leading to cell damage and apoptosis.CONCLUSION: This study provides new insights into the mechanisms of SARS-CoV-2 entry into the heart and defines promising targets for antiviral interventions for COVID-19 patients with pre-existing heart conditions or patients with co-morbidities.

KW - COVID-19

KW - Humans

KW - Inflammation

KW - Myocytes, Cardiac

KW - Oxidative Stress

KW - SARS-CoV-2

U2 - 10.1016/j.ijcard.2022.05.055

DO - 10.1016/j.ijcard.2022.05.055

M3 - SCORING: Journal article

C2 - 35643215

VL - 362

SP - 196

EP - 205

JO - INT J CARDIOL

JF - INT J CARDIOL

SN - 0167-5273

ER -