Carbon dioxide inhibits COVID-19-type proinflammatory responses through extracellular signal-regulated kinases 1 and 2, novel carbon dioxide sensors
Mitogen-activated protein kinase (MAPK) signalling pathways are crucial for developmental processes, oncogenesis, and inflammation, including the production of proinflammatory cytokines caused by reactive oxygen species and upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection....
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| Veröffentlicht in: | Cellular and molecular life sciences : CMLS 2021-12, Vol.78 (24), p.8229-8242 |
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| description | Mitogen-activated protein kinase (MAPK) signalling pathways are crucial for developmental processes, oncogenesis, and inflammation, including the production of proinflammatory cytokines caused by reactive oxygen species and upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. There are no drugs that can effectively prevent excessive inflammatory responses in endothelial cells in the lungs, heart, brain, and kidneys, which are considered the main causes of severe coronavirus disease 2019 (COVID-19). In this work, we demonstrate that human MAPKs, i.e. extracellular signal-regulated kinases 1 and 2 (ERK1/2), are CO
2
sensors and CO
2
is an efficient anti-inflammatory compound that exerts its effects through inactivating ERK1/2 in cultured endothelial cells when the CO
2
concentration is elevated. CO
2
is a potent inhibitor of cellular proinflammatory responses caused by H
2
O
2
or the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2. ERK1/2 activated by the combined action of RBD and cytokines crucial for the development of severe COVID-19, i.e. interferon-gamma (IFNγ) and tumour necrosis factor-α (TNFα), are more effectively inactivated by CO
2
than by dexamethasone or acetylsalicylic acid in human bronchial epithelial cells. Previously, many preclinical and clinical studies showed that the transient application of 5–8% CO
2
is safe and effective in the treatment of many diseases. Therefore, our research indicates that CO
2
may be used for the treatment of COVID-19 as well as the modification of hundreds of cellular pathways. |
| doi_str_mv | 10.1007/s00018-021-04005-3 |
| format | Article |
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2
sensors and CO
2
is an efficient anti-inflammatory compound that exerts its effects through inactivating ERK1/2 in cultured endothelial cells when the CO
2
concentration is elevated. CO
2
is a potent inhibitor of cellular proinflammatory responses caused by H
2
O
2
or the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2. ERK1/2 activated by the combined action of RBD and cytokines crucial for the development of severe COVID-19, i.e. interferon-gamma (IFNγ) and tumour necrosis factor-α (TNFα), are more effectively inactivated by CO
2
than by dexamethasone or acetylsalicylic acid in human bronchial epithelial cells. Previously, many preclinical and clinical studies showed that the transient application of 5–8% CO
2
is safe and effective in the treatment of many diseases. Therefore, our research indicates that CO
2
may be used for the treatment of COVID-19 as well as the modification of hundreds of cellular pathways.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-021-04005-3</identifier><identifier>PMID: 34741187</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Acetylsalicylic acid ; Activated carbon ; Anti-Inflammatory Agents - pharmacology ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Carbon dioxide ; Carbon Dioxide - pharmacology ; Carbon dioxide concentration ; Cell Biology ; Cell Line ; Coronaviruses ; COVID-19 ; COVID-19 - drug therapy ; COVID-19 - immunology ; COVID-19 - pathology ; Cytokines ; Deactivation ; Dexamethasone ; Endothelial cells ; Epithelial cells ; Epithelium ; Extracellular signal-regulated kinase ; Health services ; Human Umbilical Vein Endothelial Cells ; Humans ; Hydrogen peroxide ; Hydrogen Peroxide - toxicity ; Inflammation ; Inflammation - drug therapy ; Interferon ; Interferon-gamma - drug effects ; Kinases ; Life Sciences ; MAP kinase ; Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors ; Mitogen-Activated Protein Kinase 3 - metabolism ; Original ; Original Article ; Protein Domains - drug effects ; Protein kinase ; Proteins ; Reactive oxygen species ; SARS-CoV-2 - immunology ; Sensors ; Severe acute respiratory syndrome coronavirus 2 ; Signal transduction ; Spike Glycoprotein, Coronavirus - metabolism ; Spike protein ; Tumor Necrosis Factor-alpha - drug effects ; Tumor necrosis factor-α ; Tumorigenesis ; Tumors ; Viral diseases ; γ-Interferon</subject><ispartof>Cellular and molecular life sciences : CMLS, 2021-12, Vol.78 (24), p.8229-8242</ispartof><rights>The Author(s) 2021</rights><rights>2021. The Author(s).</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-55ad81857e929bd7d886889eae0fbfcd4308118b50868ae30756227b6f024e8e3</citedby><cites>FETCH-LOGICAL-c474t-55ad81857e929bd7d886889eae0fbfcd4308118b50868ae30756227b6f024e8e3</cites><orcidid>0000-0002-1064-426X ; 0000-0002-9639-1645 ; 0000-0001-8550-8337</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8571007/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8571007/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,41488,42557,51319,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34741187$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Galganska, Hanna</creatorcontrib><creatorcontrib>Jarmuszkiewicz, Wieslawa</creatorcontrib><creatorcontrib>Galganski, Lukasz</creatorcontrib><title>Carbon dioxide inhibits COVID-19-type proinflammatory responses through extracellular signal-regulated kinases 1 and 2, novel carbon dioxide sensors</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell. Mol. Life Sci</addtitle><addtitle>Cell Mol Life Sci</addtitle><description>Mitogen-activated protein kinase (MAPK) signalling pathways are crucial for developmental processes, oncogenesis, and inflammation, including the production of proinflammatory cytokines caused by reactive oxygen species and upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. There are no drugs that can effectively prevent excessive inflammatory responses in endothelial cells in the lungs, heart, brain, and kidneys, which are considered the main causes of severe coronavirus disease 2019 (COVID-19). In this work, we demonstrate that human MAPKs, i.e. extracellular signal-regulated kinases 1 and 2 (ERK1/2), are CO
2
sensors and CO
2
is an efficient anti-inflammatory compound that exerts its effects through inactivating ERK1/2 in cultured endothelial cells when the CO
2
concentration is elevated. CO
2
is a potent inhibitor of cellular proinflammatory responses caused by H
2
O
2
or the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2. ERK1/2 activated by the combined action of RBD and cytokines crucial for the development of severe COVID-19, i.e. interferon-gamma (IFNγ) and tumour necrosis factor-α (TNFα), are more effectively inactivated by CO
2
than by dexamethasone or acetylsalicylic acid in human bronchial epithelial cells. Previously, many preclinical and clinical studies showed that the transient application of 5–8% CO
2
is safe and effective in the treatment of many diseases. Therefore, our research indicates that CO
2
may be used for the treatment of COVID-19 as well as the modification of hundreds of cellular pathways.</description><subject>Acetylsalicylic acid</subject><subject>Activated carbon</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carbon dioxide</subject><subject>Carbon Dioxide - pharmacology</subject><subject>Carbon dioxide concentration</subject><subject>Cell Biology</subject><subject>Cell Line</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>COVID-19 - drug therapy</subject><subject>COVID-19 - immunology</subject><subject>COVID-19 - pathology</subject><subject>Cytokines</subject><subject>Deactivation</subject><subject>Dexamethasone</subject><subject>Endothelial cells</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Extracellular signal-regulated kinase</subject><subject>Health services</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>Hydrogen peroxide</subject><subject>Hydrogen Peroxide - toxicity</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Interferon</subject><subject>Interferon-gamma - drug effects</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>MAP kinase</subject><subject>Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Original</subject><subject>Original Article</subject><subject>Protein Domains - drug effects</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>SARS-CoV-2 - immunology</subject><subject>Sensors</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>Signal transduction</subject><subject>Spike Glycoprotein, Coronavirus - metabolism</subject><subject>Spike protein</subject><subject>Tumor Necrosis Factor-alpha - drug effects</subject><subject>Tumor necrosis factor-α</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Viral diseases</subject><subject>γ-Interferon</subject><issn>1420-682X</issn><issn>1420-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kctu1DAUhiMEohd4ARbIEhsWNRw7FzsbpGq4tFKlbgCxs5z4JOOS2MFOqs578MB4mGlpu2Dly_nOfy5_lr1i8I4BiPcRAJikwBmFAqCk-ZPskBUcaA2CPd3fK8l_HGRHMV4lupS8ep4d5IUoGJPiMPu90qHxjhjrb6xBYt3aNnaOZHX5_fwjZTWdNxOSKXjrukGPo5592JCAcfIuYiTzOvilXxO8mYNucRiWQQcSbe_0QAP26TmjIT-t01ucEe0M4SfE-WscSPuwekQXfYgvsmedHiK-3J_H2bfPn76uzujF5Zfz1ekFbVP_My1LbSSTpcCa140RRspKyho1Qtd0rSlykGnKpoT0rzEHUVaci6bqgBcoMT_OPux0p6UZ0bTo0gyDmoIdddgor616GHF2rXp_rVLNrQNJ4O1eIPhfC8ZZjTZul6Ad-iUqXtYFr4VkkNA3j9Arv4S0pERVUPCi5oIliu-oNvgYA3Z3zTBQ25JqZ7pKpqu_pqs8Jb2-P8Zdyq3LCch3QEwh12P4V_s_sn8AWMm6Jg</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Galganska, Hanna</creator><creator>Jarmuszkiewicz, Wieslawa</creator><creator>Galganski, Lukasz</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1064-426X</orcidid><orcidid>https://orcid.org/0000-0002-9639-1645</orcidid><orcidid>https://orcid.org/0000-0001-8550-8337</orcidid></search><sort><creationdate>20211201</creationdate><title>Carbon dioxide inhibits COVID-19-type proinflammatory responses through extracellular signal-regulated kinases 1 and 2, novel carbon dioxide sensors</title><author>Galganska, Hanna ; Jarmuszkiewicz, Wieslawa ; Galganski, Lukasz</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-55ad81857e929bd7d886889eae0fbfcd4308118b50868ae30756227b6f024e8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acetylsalicylic acid</topic><topic>Activated carbon</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Carbon dioxide</topic><topic>Carbon Dioxide - pharmacology</topic><topic>Carbon dioxide concentration</topic><topic>Cell Biology</topic><topic>Cell Line</topic><topic>Coronaviruses</topic><topic>COVID-19</topic><topic>COVID-19 - drug therapy</topic><topic>COVID-19 - immunology</topic><topic>COVID-19 - pathology</topic><topic>Cytokines</topic><topic>Deactivation</topic><topic>Dexamethasone</topic><topic>Endothelial cells</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Extracellular signal-regulated kinase</topic><topic>Health services</topic><topic>Human Umbilical Vein Endothelial Cells</topic><topic>Humans</topic><topic>Hydrogen peroxide</topic><topic>Hydrogen Peroxide - toxicity</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Interferon</topic><topic>Interferon-gamma - drug effects</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>MAP kinase</topic><topic>Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Original</topic><topic>Original Article</topic><topic>Protein Domains - drug effects</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>SARS-CoV-2 - immunology</topic><topic>Sensors</topic><topic>Severe acute respiratory syndrome coronavirus 2</topic><topic>Signal transduction</topic><topic>Spike Glycoprotein, Coronavirus - metabolism</topic><topic>Spike protein</topic><topic>Tumor Necrosis Factor-alpha - drug effects</topic><topic>Tumor necrosis factor-α</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>Viral diseases</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Galganska, Hanna</creatorcontrib><creatorcontrib>Jarmuszkiewicz, Wieslawa</creatorcontrib><creatorcontrib>Galganski, Lukasz</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Agriculture Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cellular and molecular life sciences : CMLS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Galganska, Hanna</au><au>Jarmuszkiewicz, Wieslawa</au><au>Galganski, Lukasz</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Carbon dioxide inhibits COVID-19-type proinflammatory responses through extracellular signal-regulated kinases 1 and 2, novel carbon dioxide sensors</atitle><jtitle>Cellular and molecular life sciences : CMLS</jtitle><stitle>Cell. Mol. Life Sci</stitle><addtitle>Cell Mol Life Sci</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>78</volume><issue>24</issue><spage>8229</spage><epage>8242</epage><pages>8229-8242</pages><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>Mitogen-activated protein kinase (MAPK) signalling pathways are crucial for developmental processes, oncogenesis, and inflammation, including the production of proinflammatory cytokines caused by reactive oxygen species and upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. There are no drugs that can effectively prevent excessive inflammatory responses in endothelial cells in the lungs, heart, brain, and kidneys, which are considered the main causes of severe coronavirus disease 2019 (COVID-19). In this work, we demonstrate that human MAPKs, i.e. extracellular signal-regulated kinases 1 and 2 (ERK1/2), are CO
2
sensors and CO
2
is an efficient anti-inflammatory compound that exerts its effects through inactivating ERK1/2 in cultured endothelial cells when the CO
2
concentration is elevated. CO
2
is a potent inhibitor of cellular proinflammatory responses caused by H
2
O
2
or the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2. ERK1/2 activated by the combined action of RBD and cytokines crucial for the development of severe COVID-19, i.e. interferon-gamma (IFNγ) and tumour necrosis factor-α (TNFα), are more effectively inactivated by CO
2
than by dexamethasone or acetylsalicylic acid in human bronchial epithelial cells. Previously, many preclinical and clinical studies showed that the transient application of 5–8% CO
2
is safe and effective in the treatment of many diseases. Therefore, our research indicates that CO
2
may be used for the treatment of COVID-19 as well as the modification of hundreds of cellular pathways.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>34741187</pmid><doi>10.1007/s00018-021-04005-3</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-1064-426X</orcidid><orcidid>https://orcid.org/0000-0002-9639-1645</orcidid><orcidid>https://orcid.org/0000-0001-8550-8337</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1420-682X |
| ispartof | Cellular and molecular life sciences : CMLS, 2021-12, Vol.78 (24), p.8229-8242 |
| issn | 1420-682X 1420-9071 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8571007 |
| source | MEDLINE; SpringerLink (Online service); PubMed Central |
| subjects | Acetylsalicylic acid Activated carbon Anti-Inflammatory Agents - pharmacology Biochemistry Biomedical and Life Sciences Biomedicine Carbon dioxide Carbon Dioxide - pharmacology Carbon dioxide concentration Cell Biology Cell Line Coronaviruses COVID-19 COVID-19 - drug therapy COVID-19 - immunology COVID-19 - pathology Cytokines Deactivation Dexamethasone Endothelial cells Epithelial cells Epithelium Extracellular signal-regulated kinase Health services Human Umbilical Vein Endothelial Cells Humans Hydrogen peroxide Hydrogen Peroxide - toxicity Inflammation Inflammation - drug therapy Interferon Interferon-gamma - drug effects Kinases Life Sciences MAP kinase Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors Mitogen-Activated Protein Kinase 3 - metabolism Original Original Article Protein Domains - drug effects Protein kinase Proteins Reactive oxygen species SARS-CoV-2 - immunology Sensors Severe acute respiratory syndrome coronavirus 2 Signal transduction Spike Glycoprotein, Coronavirus - metabolism Spike protein Tumor Necrosis Factor-alpha - drug effects Tumor necrosis factor-α Tumorigenesis Tumors Viral diseases γ-Interferon |
| title | Carbon dioxide inhibits COVID-19-type proinflammatory responses through extracellular signal-regulated kinases 1 and 2, novel carbon dioxide sensors |
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