Cited by 461COVID-19 Clinical Research StudiesSARS-CoV-2 and COVID-19 ResearchRenin-Angiotensin System Studies

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COVID-19 cytokine storm: The anger of inflammation

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Mahmudpour, Mehdi, Roozbeh, Jamshid, Keshavarz, Mohsen, Farrokhi, Shokrollah, Nabipour, Iraj·2020·Cytokine

DOI 10.1016/j.cyto.2020.155151PMC PMC7260598

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Abstract

Patients with COVID-19 who require ICU admission might have the cytokine storm. It is a state of out-of-control release of a variety of inflammatory cytokines. The molecular mechanism of the cytokine storm has not been explored extensively yet. The attachment of SARS-CoV-2 spike glycoprotein with angiotensin-converting enzyme 2 (ACE2), as its cellular receptor, triggers complex molecular events that leads to hyperinflammation. Four molecular axes that may be involved in SARS-CoV-2 driven inflammatory cytokine overproduction are addressed in this work. The virus-mediated down-regulation of ACE2 causes a burst of inflammatory cytokine release through dysregulation of the renin-angiotensin-aldosterone system (ACE/angiotensin II/AT1R axis), attenuation of Mas receptor (ACE2/MasR axis), increased activation of [des-Arg9]-bradykinin (ACE2/bradykinin B1R/DABK axis), and activation of the complement system including C5a and C5b-9 components. The molecular clarification of these axes will elucidate an array of therapeutic strategies to confront the cytokine storm in order to prevent and treat COVID-19 associated acute respiratory distress syndrome.

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“Cytokine storm was a phenomenon linked to the increased levels of ferritin, CRP, and other inflammatory blood biomarkers [38, 39], as well as ARDS, a phenomenon that identified patients in critical COVID-19 state [40], further worsening to ICU support and ultimately death [41].”
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Deus, M. D. C., Gadotti, A. C., Dias, E. S., Alegre, J. B. M., Spitzenbergen, B. A. K. V., Bohnen, G., Tozoni, S. S., Stocco, R. B., Olandoski, M., Tuon, F. F., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms251910578 · Cited by 7
“Virus binding to the ACE2 receptor also induces TGF-β expression [23,24], promoting differentiation of naive CD4+ T cells into T helper 17 (Th-17) cells, which produce cytokines like IL-17, GM-CSF, IL-21, and IL-2 [25].”
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Atemnkeng, F. N., Alataby, H., Demirjian, J., Kenne, F. M., & Nfonoyim, J. M. (2021) · Journal of Medical Cases · doi:10.14740/jmc3629 · Cited by 6
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“immune response produced by the body to external stimuli, such as viral infection, and is characterized by high levels of immune cell activation and subsequent production of large amounts of cytokines and chemical mediators [5].”
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“In this COVID-19 pandemic, the current evidence indicates that inflammation is a prominent pathophysiological process (59), with acute respiratory distress syndrome (ARDS) observed in over 70% of ICU patients and 90% of nonsurvivors (60).”

Authors: Mahmudpour, M., Roozbeh, J., Keshavarz, M., Farrokhi, S., & Nabipour, I.
Affiliations: Bushehr University of Medical Sciences (IR)
Shiraz University of Medical Sciences (IR)
Iranian Academy of Medical Sciences (IR)
Corresponding author: Nabipour, Iraj
ORCID: Mahmudpour, Mehdi
Roozbeh, Jamshid
Keshavarz, Mohsen
Farrokhi, Shokrollah
Nabipour, Iraj
Venue: Cytokine
Publisher: Elsevier BV
Published: 2020-09
Volume: 133
Pages: 155151
ISSN: 1043-4666 (ISSN-L)
DOI: 10.1016/j.cyto.2020.155151
PMC: PMC7260598
OpenAlex: W3030136428
Cited by: 461
References: 140
Citations by year: 2026: 8 · 2025: 18 · 2024: 47 · 2023: 61 · 2022: 104 · 2021: 168 · 2020: 52
FWCI: 4.55
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Cytokine (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Bushehr University of Medical Sciences
Topics: Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Keywords: COVID-19 pandemic, cytokine storm, SARS-CoV-2, hyperinflammation, ACE2, renin-angiotensin-aldosterone system, Mas receptor, bradykinin B1 receptor, complement system, C5a, membrane attack complex, acute respiratory distress syndrome, intensive care unit patients, treatment options
MeSH terms: Betacoronavirus, Angiotensin-Converting Enzyme 2, COVID-19, SARS-CoV-2, Proto-Oncogene Mas, Bradykinin, Humans, Inflammation, Peptidyl-Dipeptidase A, Models, Molecular, Pneumonia, Viral, Proto-Oncogene Proteins, Renin-Angiotensin System, Complement C5a, Cytokines, Coronavirus Infections, Receptors, G-Protein-Coupled, Complement C5b, Pandemics, Spike Glycoprotein, Coronavirus

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COVID-19 cytokine storm: The anger of inflammation

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