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10.1042/CS20200492 http://scihub22266oqcxt.onion/10.1042/CS20200492 32507883!7276636!32507883     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32507883&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Clin+Sci+(Lond) 2020 ; 134 (11): 1259-1264 Nephropedia Template TP {{tp|p=32507883|t=2020. Covid-19: the renin-angiotensin system imbalance hypothesis |pdf=|usr=}}{{32507883}} gab.com Text Covid-19: the renin-angiotensin system imbalance hypothesis JO: Clin Sci (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=32507883 #FOAvip The emergency of SARS-CoV-2 in China started a novel challenge to the scientific community. As the virus turns pandemic, scientists try to map the cellular mechanisms and pathways of SARS-CoV-2 related to the pathogenesis of Coronavirus Disease 2019 (Covid-19). After transmembrane angiotensin-converting enzyme 2 (ACE2) has been found to be SARS-CoV-2 receptor, we hypothesized an immune-hematological mechanism for Covid-19 based on renin-angiotensin system (RAS) imbalance to explain clinical, laboratory and imaging findings on disease course. We believe that exaggerated activation of ACE/Angiotensin II (Ang II)/Angiotensin Type 1 (AT1) receptor RAS axis in line with reduction of ACE2/Angiotensin-(1-7)/Mas receptor may exert a pivotal role in the pathogenesis of Covid-19. In this perspective, we discuss potential mechanisms and evidence on this hypothesis. Twit Text FOAVip Covid-19: the renin-angiotensin system imbalance hypothesis ????Clin Sci (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=32507883 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32507883 #FOAvip English Wikipedia <ref>{{Cite pmid|32507883}}</ref> Covid-19: the renin-angiotensin system imbalance hypothesis #MMPMID32507883 Lanza K; Perez LG; Costa LB; Cordeiro TM; Palmeira VA; Ribeiro VT; Simoes E Silva AC Clin Sci (Lond) 2020[Jun]; 134 (11): 1259-1264 PMID32507883show ga The emergency of SARS-CoV-2 in China started a novel challenge to the scientific community. As the virus turns pandemic, scientists try to map the cellular mechanisms and pathways of SARS-CoV-2 related to the pathogenesis of Coronavirus Disease 2019 (Covid-19). After transmembrane angiotensin-converting enzyme 2 (ACE2) has been found to be SARS-CoV-2 receptor, we hypothesized an immune-hematological mechanism for Covid-19 based on renin-angiotensin system (RAS) imbalance to explain clinical, laboratory and imaging findings on disease course. We believe that exaggerated activation of ACE/Angiotensin II (Ang II)/Angiotensin Type 1 (AT1) receptor RAS axis in line with reduction of ACE2/Angiotensin-(1-7)/Mas receptor may exert a pivotal role in the pathogenesis of Covid-19. In this perspective, we discuss potential mechanisms and evidence on this hypothesis. |Angiotensin-Converting Enzyme 2[MESH] |Angiotensin-Converting Enzyme Inhibitors/*pharmacology[MESH] |Animals[MESH] |Betacoronavirus/*metabolism[MESH] |COVID-19[MESH] |Coronavirus Infections/*drug therapy/metabolism/virology[MESH] |Humans[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/*metabolism[MESH] |Pneumonia, Viral/*drug therapy/metabolism/virology[MESH] |Renin-Angiotensin System/*physiology[MESH]Covid-19: the renin-angiotensin system imbalance hypothesis (epmc).pdf DeepDyve Pubget Overpricing