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10.1177/0271678X20985666 http://scihub22266oqcxt.onion/10.1177/0271678X20985666 33530831!8142132!33530831     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cereb+Blood+Flow+Metab 2021 ; 41 (6): 1179-1192 Nephropedia Template TP {{tp|p=33530831|t=2021. Pathophysiologic mechanisms of cerebral endotheliopathy and stroke due to Sars-CoV-2 |pdf=|usr=}}{{33530831}} gab.com Text Pathophysiologic mechanisms of cerebral endotheliopathy and stroke due to Sars-CoV-2 JO: J Cereb Blood Flow Metab http://www.kidney.de/pget.php?&tw=1&pmid=33530831 #FOAvip Cerebrovascular events have emerged as a central feature of the clinical syndrome associated with Sars-CoV-2 infection. This increase in infection-related strokes is marked by atypical presentations including stroke in younger patients and a high rate of hemorrhagic transformation after ischemia. A variety of pathogenic mechanisms may underlie this connection. Efforts to identify synergism in the pathophysiology underlying stroke and Sars-CoV-2 infection can inform the understanding of both conditions in novel ways. In this review, the molecular cascades connected to Sars-CoV-2 infection are placed in the context of the cerebral vasculature and in relationship to pathways known to be associated with stroke. Cytokine-mediated promotion of systemic hypercoagulability is suggested while direct Sars-CoV-2 infection of cerebral endothelial cells may also contribute. Endotheliopathy resulting from direct Sars-CoV-2 infection of the cerebral vasculature can modulate ACE2/AT(1)R/MasR signaling pathways, trigger direct viral activation of the complement cascade, and activate feed-forward cytokine cascades that impact the blood-brain barrier. All of these pathways are already implicated as independent mechanisms driving stroke and cerebrovascular injury irrespective of Sars-CoV-2. Recognizing the overlap of molecular pathways triggered by Sars-CoV-2 infection with those implicated in the pathogenesis of stroke provides an opportunity to identify future therapeutics targeting both Sars-CoV-2 and stroke thereby reducing the impact of the global pandemic. Twit Text FOAVip Pathophysiologic mechanisms of cerebral endotheliopathy and stroke due to Sars-CoV-2 ????J Cereb Blood Flow Metab http://www.kidney.de/pget.php?&tw=1&pmid=33530831 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33530831 #FOAvip English Wikipedia <ref>{{Cite pmid|33530831}}</ref> Pathophysiologic mechanisms of cerebral endotheliopathy and stroke due to Sars-CoV-2 #MMPMID33530831 Kakarla V; Kaneko N; Nour M; Khatibi K; Elahi F; Liebeskind DS; Hinman JD J Cereb Blood Flow Metab 2021[Jun]; 41 (6): 1179-1192 PMID33530831show ga Cerebrovascular events have emerged as a central feature of the clinical syndrome associated with Sars-CoV-2 infection. This increase in infection-related strokes is marked by atypical presentations including stroke in younger patients and a high rate of hemorrhagic transformation after ischemia. A variety of pathogenic mechanisms may underlie this connection. Efforts to identify synergism in the pathophysiology underlying stroke and Sars-CoV-2 infection can inform the understanding of both conditions in novel ways. In this review, the molecular cascades connected to Sars-CoV-2 infection are placed in the context of the cerebral vasculature and in relationship to pathways known to be associated with stroke. Cytokine-mediated promotion of systemic hypercoagulability is suggested while direct Sars-CoV-2 infection of cerebral endothelial cells may also contribute. Endotheliopathy resulting from direct Sars-CoV-2 infection of the cerebral vasculature can modulate ACE2/AT(1)R/MasR signaling pathways, trigger direct viral activation of the complement cascade, and activate feed-forward cytokine cascades that impact the blood-brain barrier. All of these pathways are already implicated as independent mechanisms driving stroke and cerebrovascular injury irrespective of Sars-CoV-2. Recognizing the overlap of molecular pathways triggered by Sars-CoV-2 infection with those implicated in the pathogenesis of stroke provides an opportunity to identify future therapeutics targeting both Sars-CoV-2 and stroke thereby reducing the impact of the global pandemic. |Angiotensin-Converting Enzyme 2/metabolism[MESH] |Blood-Brain Barrier/metabolism[MESH] |COVID-19/complications/*pathology/virology[MESH] |Cerebrovascular Disorders/*etiology/metabolism[MESH] |Complement Activation[MESH] |Humans[MESH] |Proto-Oncogene Mas[MESH] |Renin-Angiotensin System[MESH] |Spike Glycoprotein, Coronavirus/metabolism[MESH] |Stroke/*etiology/metabolism[MESH]Pathophysiologic mechanisms of cerebral endotheliopathy and stroke due(epmc).pdf DeepDyve Pubget Overpricing