Cross-Talk Between Key Players in Patients with COVID-19 and Ischemic Stroke: A Review on Neurobiological Insight of the Pandemic
The global pandemic of novel coronavirus disease 2019 (COVID-19) has taken the entire human race by surprise and led to an unprecedented number of mortalities worldwide so far. Current clinical studies have interpreted that angiotensin-converting enzyme 2 (ACE2) is the host receptor for severe acute...
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| Veröffentlicht in: | Molecular neurobiology 2020-12, Vol.57 (12), p.4921-4928 |
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| description | The global pandemic of novel coronavirus disease 2019 (COVID-19) has taken the entire human race by surprise and led to an unprecedented number of mortalities worldwide so far. Current clinical studies have interpreted that angiotensin-converting enzyme 2 (ACE2) is the host receptor for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). In addition, ACE2 is the major component of the renin-angiotensin system. ACE2 deteriorates angiotensin II, a peptide that is responsible for the promotion of stroke. The downregulation of ACE2 further activates an immunological cascade. Thus, researchers need to explore and examine the possible links between COVID-19 and ischemic stroke (IS). Human ACE2 expression level and pattern in various tissues might be decisive for the vulnerability, symptoms, and treatment outcomes of the SARS-CoV-2 infection. The swift increase in the knowledge of SARS-CoV-2 has given creditable evidence that SARS-CoV-2 infected patients also encounter neurological deficits. As the SARS-CoV-2 binds to ACE2, it will hamper the activity of ACE2 in providing neuroprotection, especially in the case of stroke patients. Due to the downregulation of ACE2, the inflammatory response is activated in the ischemic penumbra. The COVID-19 pandemic has affected people with various pre-existing diseases, including IS, in such a way that these patients need special care and attention for their survival. Several clinical trials are currently ongoing worldwide as well as many other projects are in different stages of conceptualization and planning to facilitate the effective management of stroke patients with COVID-19 infection. |
| doi_str_mv | 10.1007/s12035-020-02072-4 |
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Current clinical studies have interpreted that angiotensin-converting enzyme 2 (ACE2) is the host receptor for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). In addition, ACE2 is the major component of the renin-angiotensin system. ACE2 deteriorates angiotensin II, a peptide that is responsible for the promotion of stroke. The downregulation of ACE2 further activates an immunological cascade. Thus, researchers need to explore and examine the possible links between COVID-19 and ischemic stroke (IS). Human ACE2 expression level and pattern in various tissues might be decisive for the vulnerability, symptoms, and treatment outcomes of the SARS-CoV-2 infection. The swift increase in the knowledge of SARS-CoV-2 has given creditable evidence that SARS-CoV-2 infected patients also encounter neurological deficits. As the SARS-CoV-2 binds to ACE2, it will hamper the activity of ACE2 in providing neuroprotection, especially in the case of stroke patients. Due to the downregulation of ACE2, the inflammatory response is activated in the ischemic penumbra. The COVID-19 pandemic has affected people with various pre-existing diseases, including IS, in such a way that these patients need special care and attention for their survival. Several clinical trials are currently ongoing worldwide as well as many other projects are in different stages of conceptualization and planning to facilitate the effective management of stroke patients with COVID-19 infection.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-020-02072-4</identifier><identifier>PMID: 32813238</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>ACE2 ; Angiotensin ; Angiotensin II ; Angiotensin-Converting Enzyme 2 ; Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Betacoronavirus - pathogenicity ; Betacoronavirus - physiology ; Biomedical and Life Sciences ; Biomedicine ; Blood-Brain Barrier ; Brain Ischemia - epidemiology ; Brain Ischemia - etiology ; Brain Ischemia - immunology ; Brain Ischemia - physiopathology ; Cell Biology ; Chemotaxis, Leukocyte ; Clinical trials ; Comorbidity ; Coronavirus Infections - complications ; Coronavirus Infections - epidemiology ; Coronavirus Infections - physiopathology ; Coronaviruses ; COVID-19 ; Cytokine Release Syndrome - etiology ; Cytokine Release Syndrome - physiopathology ; Cytokines - physiology ; Down-regulation ; Encephalitis, Viral - complications ; Encephalitis, Viral - physiopathology ; Hemodynamics ; Humans ; Inflammation ; Ischemia ; Medical treatment ; Models, Immunological ; Models, Neurological ; Multiple Organ Failure - etiology ; Multiple Organ Failure - physiopathology ; Nervous System Diseases - epidemiology ; Nervous System Diseases - etiology ; Neurobiology ; Neurological diseases ; Neurology ; Neuroprotection ; Neurosciences ; Pandemics ; Patients ; Peptidyl-dipeptidase A ; Peptidyl-Dipeptidase A - physiology ; Pneumonia, Viral - complications ; Pneumonia, Viral - epidemiology ; Pneumonia, Viral - physiopathology ; Receptors, Virus - physiology ; Renin ; Renin-Angiotensin System - physiology ; Risk ; SARS-CoV-2 ; Severe acute respiratory syndrome coronavirus 2 ; Stroke ; Stroke - epidemiology ; Stroke - etiology ; Stroke - immunology ; Stroke - physiopathology</subject><ispartof>Molecular neurobiology, 2020-12, Vol.57 (12), p.4921-4928</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-3f24494d58b690cc472de90942e292fbebe60c8ffa166fa5269fac413ae558da3</citedby><cites>FETCH-LOGICAL-c474t-3f24494d58b690cc472de90942e292fbebe60c8ffa166fa5269fac413ae558da3</cites><orcidid>0000-0002-6318-6506</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-020-02072-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-020-02072-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32813238$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kaushik, Pooja</creatorcontrib><creatorcontrib>Kaushik, Medha</creatorcontrib><creatorcontrib>Parveen, Sabiha</creatorcontrib><creatorcontrib>Tabassum, Heena</creatorcontrib><creatorcontrib>Parvez, Suhel</creatorcontrib><title>Cross-Talk Between Key Players in Patients with COVID-19 and Ischemic Stroke: A Review on Neurobiological Insight of the Pandemic</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>The global pandemic of novel coronavirus disease 2019 (COVID-19) has taken the entire human race by surprise and led to an unprecedented number of mortalities worldwide so far. Current clinical studies have interpreted that angiotensin-converting enzyme 2 (ACE2) is the host receptor for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). In addition, ACE2 is the major component of the renin-angiotensin system. ACE2 deteriorates angiotensin II, a peptide that is responsible for the promotion of stroke. The downregulation of ACE2 further activates an immunological cascade. Thus, researchers need to explore and examine the possible links between COVID-19 and ischemic stroke (IS). Human ACE2 expression level and pattern in various tissues might be decisive for the vulnerability, symptoms, and treatment outcomes of the SARS-CoV-2 infection. The swift increase in the knowledge of SARS-CoV-2 has given creditable evidence that SARS-CoV-2 infected patients also encounter neurological deficits. As the SARS-CoV-2 binds to ACE2, it will hamper the activity of ACE2 in providing neuroprotection, especially in the case of stroke patients. Due to the downregulation of ACE2, the inflammatory response is activated in the ischemic penumbra. The COVID-19 pandemic has affected people with various pre-existing diseases, including IS, in such a way that these patients need special care and attention for their survival. Several clinical trials are currently ongoing worldwide as well as many other projects are in different stages of conceptualization and planning to facilitate the effective management of stroke patients with COVID-19 infection.</description><subject>ACE2</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin-Converting Enzyme 2</subject><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Betacoronavirus - pathogenicity</subject><subject>Betacoronavirus - physiology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood-Brain Barrier</subject><subject>Brain Ischemia - epidemiology</subject><subject>Brain Ischemia - etiology</subject><subject>Brain Ischemia - immunology</subject><subject>Brain Ischemia - physiopathology</subject><subject>Cell Biology</subject><subject>Chemotaxis, Leukocyte</subject><subject>Clinical trials</subject><subject>Comorbidity</subject><subject>Coronavirus Infections - complications</subject><subject>Coronavirus Infections - epidemiology</subject><subject>Coronavirus Infections - physiopathology</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>Cytokine Release Syndrome - etiology</subject><subject>Cytokine Release Syndrome - physiopathology</subject><subject>Cytokines - physiology</subject><subject>Down-regulation</subject><subject>Encephalitis, Viral - complications</subject><subject>Encephalitis, Viral - physiopathology</subject><subject>Hemodynamics</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Medical treatment</subject><subject>Models, Immunological</subject><subject>Models, Neurological</subject><subject>Multiple Organ Failure - etiology</subject><subject>Multiple Organ Failure - physiopathology</subject><subject>Nervous System Diseases - epidemiology</subject><subject>Nervous System Diseases - etiology</subject><subject>Neurobiology</subject><subject>Neurological diseases</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>Pandemics</subject><subject>Patients</subject><subject>Peptidyl-dipeptidase A</subject><subject>Peptidyl-Dipeptidase A - 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therapeutic use</topic><topic>Betacoronavirus - pathogenicity</topic><topic>Betacoronavirus - physiology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood-Brain Barrier</topic><topic>Brain Ischemia - epidemiology</topic><topic>Brain Ischemia - etiology</topic><topic>Brain Ischemia - immunology</topic><topic>Brain Ischemia - physiopathology</topic><topic>Cell Biology</topic><topic>Chemotaxis, Leukocyte</topic><topic>Clinical trials</topic><topic>Comorbidity</topic><topic>Coronavirus Infections - complications</topic><topic>Coronavirus Infections - epidemiology</topic><topic>Coronavirus Infections - physiopathology</topic><topic>Coronaviruses</topic><topic>COVID-19</topic><topic>Cytokine Release Syndrome - etiology</topic><topic>Cytokine Release Syndrome - physiopathology</topic><topic>Cytokines - physiology</topic><topic>Down-regulation</topic><topic>Encephalitis, Viral - complications</topic><topic>Encephalitis, Viral - physiopathology</topic><topic>Hemodynamics</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>Medical treatment</topic><topic>Models, Immunological</topic><topic>Models, Neurological</topic><topic>Multiple Organ Failure - 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Current clinical studies have interpreted that angiotensin-converting enzyme 2 (ACE2) is the host receptor for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). In addition, ACE2 is the major component of the renin-angiotensin system. ACE2 deteriorates angiotensin II, a peptide that is responsible for the promotion of stroke. The downregulation of ACE2 further activates an immunological cascade. Thus, researchers need to explore and examine the possible links between COVID-19 and ischemic stroke (IS). Human ACE2 expression level and pattern in various tissues might be decisive for the vulnerability, symptoms, and treatment outcomes of the SARS-CoV-2 infection. The swift increase in the knowledge of SARS-CoV-2 has given creditable evidence that SARS-CoV-2 infected patients also encounter neurological deficits. As the SARS-CoV-2 binds to ACE2, it will hamper the activity of ACE2 in providing neuroprotection, especially in the case of stroke patients. Due to the downregulation of ACE2, the inflammatory response is activated in the ischemic penumbra. The COVID-19 pandemic has affected people with various pre-existing diseases, including IS, in such a way that these patients need special care and attention for their survival. Several clinical trials are currently ongoing worldwide as well as many other projects are in different stages of conceptualization and planning to facilitate the effective management of stroke patients with COVID-19 infection.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32813238</pmid><doi>10.1007/s12035-020-02072-4</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-6318-6506</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | ACE2 Angiotensin Angiotensin II Angiotensin-Converting Enzyme 2 Angiotensin-Converting Enzyme Inhibitors - therapeutic use Betacoronavirus - pathogenicity Betacoronavirus - physiology Biomedical and Life Sciences Biomedicine Blood-Brain Barrier Brain Ischemia - epidemiology Brain Ischemia - etiology Brain Ischemia - immunology Brain Ischemia - physiopathology Cell Biology Chemotaxis, Leukocyte Clinical trials Comorbidity Coronavirus Infections - complications Coronavirus Infections - epidemiology Coronavirus Infections - physiopathology Coronaviruses COVID-19 Cytokine Release Syndrome - etiology Cytokine Release Syndrome - physiopathology Cytokines - physiology Down-regulation Encephalitis, Viral - complications Encephalitis, Viral - physiopathology Hemodynamics Humans Inflammation Ischemia Medical treatment Models, Immunological Models, Neurological Multiple Organ Failure - etiology Multiple Organ Failure - physiopathology Nervous System Diseases - epidemiology Nervous System Diseases - etiology Neurobiology Neurological diseases Neurology Neuroprotection Neurosciences Pandemics Patients Peptidyl-dipeptidase A Peptidyl-Dipeptidase A - physiology Pneumonia, Viral - complications Pneumonia, Viral - epidemiology Pneumonia, Viral - physiopathology Receptors, Virus - physiology Renin Renin-Angiotensin System - physiology Risk SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 Stroke Stroke - epidemiology Stroke - etiology Stroke - immunology Stroke - physiopathology |
| title | Cross-Talk Between Key Players in Patients with COVID-19 and Ischemic Stroke: A Review on Neurobiological Insight of the Pandemic |
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