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The key role of Calpain in COVID-19 as a therapeutic strategy

COVID-19 is one of the viral diseases that has caused many deaths and financial losses to humans. Using the available information, this virus appears to activate the host cell-death mechanism through Calpain activation. Calpain inhibition can stop its downstream cascade reactions that cause cell dea...

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Detalles Bibliográficos
Autores principales: Juibari, Aref Doozandeh, Rezadoost, Mohammad Hossein, Soleimani, Masoud
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9149670/
https://www.ncbi.nlm.nih.gov/pubmed/35635676
http://dx.doi.org/10.1007/s10787-022-01002-1
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author Juibari, Aref Doozandeh
Rezadoost, Mohammad Hossein
Soleimani, Masoud
author_facet Juibari, Aref Doozandeh
Rezadoost, Mohammad Hossein
Soleimani, Masoud
author_sort Juibari, Aref Doozandeh
collection PubMed
description COVID-19 is one of the viral diseases that has caused many deaths and financial losses to humans. Using the available information, this virus appears to activate the host cell-death mechanism through Calpain activation. Calpain inhibition can stop its downstream cascade reactions that cause cell death. Given the main roles of Calpain in the entry and pathogenicity of the SARS-CoV-2, its inhibition can be effective in controlling the COVID-19. This review describes how the virus activates Calpain by altering calcium flow. When Calpain was activated, the virus can enter the target cell. Subsequently, many complications of the disease, such as inflammation, cytokine storm and pulmonary fibrosis, are caused by virus-activated Calpain function. Calpain inhibitors appear to be a potential drug to control the disease and prevent death from COVID-19.
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spelling pubmed-91496702022-06-02 The key role of Calpain in COVID-19 as a therapeutic strategy Juibari, Aref Doozandeh Rezadoost, Mohammad Hossein Soleimani, Masoud Inflammopharmacology Review COVID-19 is one of the viral diseases that has caused many deaths and financial losses to humans. Using the available information, this virus appears to activate the host cell-death mechanism through Calpain activation. Calpain inhibition can stop its downstream cascade reactions that cause cell death. Given the main roles of Calpain in the entry and pathogenicity of the SARS-CoV-2, its inhibition can be effective in controlling the COVID-19. This review describes how the virus activates Calpain by altering calcium flow. When Calpain was activated, the virus can enter the target cell. Subsequently, many complications of the disease, such as inflammation, cytokine storm and pulmonary fibrosis, are caused by virus-activated Calpain function. Calpain inhibitors appear to be a potential drug to control the disease and prevent death from COVID-19. Springer International Publishing 2022-05-30 2022 /pmc/articles/PMC9149670/ /pubmed/35635676 http://dx.doi.org/10.1007/s10787-022-01002-1 Text en © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Review
Juibari, Aref Doozandeh
Rezadoost, Mohammad Hossein
Soleimani, Masoud
The key role of Calpain in COVID-19 as a therapeutic strategy
title The key role of Calpain in COVID-19 as a therapeutic strategy
title_full The key role of Calpain in COVID-19 as a therapeutic strategy
title_fullStr The key role of Calpain in COVID-19 as a therapeutic strategy
title_full_unstemmed The key role of Calpain in COVID-19 as a therapeutic strategy
title_short The key role of Calpain in COVID-19 as a therapeutic strategy
title_sort key role of calpain in covid-19 as a therapeutic strategy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9149670/
https://www.ncbi.nlm.nih.gov/pubmed/35635676
http://dx.doi.org/10.1007/s10787-022-01002-1
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