CovidStanfordV1, Main, Exploration, bibRecord, 000140

p38 MAPK inhibition: A promising therapeutic approach for COVID-19.

Identifieur interne : 000140 ( Main/Exploration ); précédent : 000139; suivant : 000141

p38 MAPK inhibition: A promising therapeutic approach for COVID-19.

Auteurs : Joseph M. Grimes [États-Unis] ; Kevin V. Grimes [États-Unis]

Source :

Journal of molecular and cellular cardiology [ 1095-8584 ] ; 2020.

RBID : pubmed:32422320

Descripteurs français

KwdFr :
- Activation enzymatique (MeSH), Animaux (MeSH), Antiviraux (pharmacologie), Betacoronavirus (pathogénicité), Humains (MeSH), Infections à coronavirus (enzymologie), Infections à coronavirus (traitement médicamenteux), Inflammation (traitement médicamenteux), Inflammation (virologie), Inhibiteurs de protéines kinases (pharmacologie), Interactions hôte-pathogène (physiologie), Pandémies (MeSH), Pneumopathie virale (enzymologie), Pneumopathie virale (traitement médicamenteux), Poumon (métabolisme), Poumon (physiopathologie), Poumon (virologie), p38 Mitogen-Activated Protein Kinases (antagonistes et inhibiteurs), p38 Mitogen-Activated Protein Kinases (métabolisme).
MESH :
- antagonistes et inhibiteurs : p38 Mitogen-Activated Protein Kinases.
- enzymologie : Infections à coronavirus, Pneumopathie virale.
- métabolisme : Poumon, p38 Mitogen-Activated Protein Kinases.
- pathogénicité : Betacoronavirus.
- pharmacologie : Antiviraux, Inhibiteurs de protéines kinases.
- physiologie : Interactions hôte-pathogène.
- physiopathologie : Poumon.
- traitement médicamenteux : Infections à coronavirus, Inflammation, Pneumopathie virale.
- virologie : Inflammation, Poumon.
- Activation enzymatique, Animaux, Humains, Pandémies.

English descriptors

KwdEn :
- Animals (MeSH), Antiviral Agents (pharmacology), Betacoronavirus (pathogenicity), COVID-19 (MeSH), Coronavirus Infections (drug therapy), Coronavirus Infections (enzymology), Enzyme Activation (MeSH), Host-Pathogen Interactions (physiology), Humans (MeSH), Inflammation (drug therapy), Inflammation (virology), Lung (metabolism), Lung (physiopathology), Lung (virology), Pandemics (MeSH), Pneumonia, Viral (drug therapy), Pneumonia, Viral (enzymology), Protein Kinase Inhibitors (pharmacology), SARS-CoV-2 (MeSH), p38 Mitogen-Activated Protein Kinases (antagonists & inhibitors), p38 Mitogen-Activated Protein Kinases (metabolism).
MESH :
- chemical , antagonists & inhibitors : p38 Mitogen-Activated Protein Kinases.
- chemical , metabolism : p38 Mitogen-Activated Protein Kinases.
- chemical , pharmacology : Antiviral Agents, Protein Kinase Inhibitors.
- drug therapy : Coronavirus Infections, Inflammation, Pneumonia, Viral.
- enzymology : Coronavirus Infections, Pneumonia, Viral.
- metabolism : Lung.
- pathogenicity : Betacoronavirus.
- physiology : Host-Pathogen Interactions.
- physiopathology : Lung.
- virology : Inflammation, Lung.
- Animals, COVID-19, Enzyme Activation, Humans, Pandemics, SARS-CoV-2.

Abstract

COVID-19, caused by the SARS-CoV-2 virus, is a major source of morbidity and mortality due to its inflammatory effects in the lungs and heart. The p38 MAPK pathway plays a crucial role in the release of pro-inflammatory cytokines such as IL-6 and has been implicated in acute lung injury and myocardial dysfunction. The overwhelming inflammatory response in COVID-19 infection may be caused by disproportionately upregulated p38 activity, explained by two mechanisms. First, angiotensin-converting enzyme 2 (ACE2) activity is lost during SARS-CoV-2 viral entry. ACE2 is highly expressed in the lungs and heart and converts Angiotensin II into Angiotensin 1-7. Angiotensin II signals proinflammatory, pro-vasoconstrictive, pro-thrombotic activity through p38 MAPK activation, which is countered by Angiotensin 1-7 downregulation of p38 activity. Loss of ACE2 upon viral entry may tip the balance towards destructive p38 signaling through Angiotensin II. Second, SARS-CoV was previously shown to directly upregulate p38 activity via a viral protein, similar to other RNA respiratory viruses that may hijack p38 activity to promote replication. Given the homology between SARS-CoV and SARS-CoV-2, the latter may employ a similar mechanism. Thus, SARS-CoV-2 may induce overwhelming inflammation by directly activating p38 and downregulating a key inhibitory pathway, while simultaneously taking advantage of p38 activity to replicate. Therapeutic inhibition of p38 could therefore attenuate COVID-19 infection. Interestingly, a prior preclinical study showed protective effects of p38 inhibition in a SARS-CoV mouse model. A number of p38 inhibitors are in the clinical stage and should be considered for clinical trials in serious COVID-19 infection.

DOI: 10.1016/j.yjmcc.2020.05.007
PubMed: 32422320
PubMed Central: PMC7228886

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000711
to stream Main, to step Curation: 000711

Le document en format XML

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<front><div type="abstract" xml:lang="en">COVID-19, caused by the SARS-CoV-2 virus, is a major source of morbidity and mortality due to its inflammatory effects in the lungs and heart. The p38 MAPK pathway plays a crucial role in the release of pro-inflammatory cytokines such as IL-6 and has been implicated in acute lung injury and myocardial dysfunction. The overwhelming inflammatory response in COVID-19 infection may be caused by disproportionately upregulated p38 activity, explained by two mechanisms. First, angiotensin-converting enzyme 2 (ACE2) activity is lost during SARS-CoV-2 viral entry. ACE2 is highly expressed in the lungs and heart and converts Angiotensin II into Angiotensin 1-7. Angiotensin II signals proinflammatory, pro-vasoconstrictive, pro-thrombotic activity through p38 MAPK activation, which is countered by Angiotensin 1-7 downregulation of p38 activity. Loss of ACE2 upon viral entry may tip the balance towards destructive p38 signaling through Angiotensin II. Second, SARS-CoV was previously shown to directly upregulate p38 activity via a viral protein, similar to other RNA respiratory viruses that may hijack p38 activity to promote replication. Given the homology between SARS-CoV and SARS-CoV-2, the latter may employ a similar mechanism. Thus, SARS-CoV-2 may induce overwhelming inflammation by directly activating p38 and downregulating a key inhibitory pathway, while simultaneously taking advantage of p38 activity to replicate. Therapeutic inhibition of p38 could therefore attenuate COVID-19 infection. Interestingly, a prior preclinical study showed protective effects of p38 inhibition in a SARS-CoV mouse model. A number of p38 inhibitors are in the clinical stage and should be considered for clinical trials in serious COVID-19 infection.</div>
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<Abstract><AbstractText>COVID-19, caused by the SARS-CoV-2 virus, is a major source of morbidity and mortality due to its inflammatory effects in the lungs and heart. The p38 MAPK pathway plays a crucial role in the release of pro-inflammatory cytokines such as IL-6 and has been implicated in acute lung injury and myocardial dysfunction. The overwhelming inflammatory response in COVID-19 infection may be caused by disproportionately upregulated p38 activity, explained by two mechanisms. First, angiotensin-converting enzyme 2 (ACE2) activity is lost during SARS-CoV-2 viral entry. ACE2 is highly expressed in the lungs and heart and converts Angiotensin II into Angiotensin 1-7. Angiotensin II signals proinflammatory, pro-vasoconstrictive, pro-thrombotic activity through p38 MAPK activation, which is countered by Angiotensin 1-7 downregulation of p38 activity. Loss of ACE2 upon viral entry may tip the balance towards destructive p38 signaling through Angiotensin II. Second, SARS-CoV was previously shown to directly upregulate p38 activity via a viral protein, similar to other RNA respiratory viruses that may hijack p38 activity to promote replication. Given the homology between SARS-CoV and SARS-CoV-2, the latter may employ a similar mechanism. Thus, SARS-CoV-2 may induce overwhelming inflammation by directly activating p38 and downregulating a key inhibitory pathway, while simultaneously taking advantage of p38 activity to replicate. Therapeutic inhibition of p38 could therefore attenuate COVID-19 infection. Interestingly, a prior preclinical study showed protective effects of p38 inhibition in a SARS-CoV mouse model. A number of p38 inhibitors are in the clinical stage and should be considered for clinical trials in serious COVID-19 infection.</AbstractText>
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p38 MAPK inhibition: A promising therapeutic approach for COVID-19.

p38 MAPK inhibition: A promising therapeutic approach for COVID-19.

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