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suck abstract from ncbi


10.2174/1389450121666201020154033

http://scihub22266oqcxt.onion/10.2174/1389450121666201020154033
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33081670!ä!33081670

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suck abstract from ncbi


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pmid33081670      Curr+Drug+Targets 2021 ; 22 (3): 254-281
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  • Downregulation of Membrane-bound Angiotensin Converting Enzyme 2 (ACE2) Receptor has a Pivotal Role in COVID-19 Immunopathology #MMPMID33081670
  • Vieira C; Nery L; Martins L; Jabour L; Dias R; Simoes E Silva AC
  • Curr Drug Targets 2021[]; 22 (3): 254-281 PMID33081670show ga
  • BACKGROUND: The Coronavirus Disease 2019 (COVID-19) is becoming the major health issue in recent human history with thousands of deaths and millions of cases worldwide. Newer research and old experience with other coronaviruses highlighted a probable underlying mechanism of disturbance of the renin-angiotensin system (RAS) that is associated with the intrinsic effects of SARS-CoV-2 infection. OBJECTIVE: In this review, we aimed to describe the intimate connections between the RAS components, the immune system and COVID-19 pathophysiology. METHODS: This non-systematic review article summarizes recent evidence on the relationship between COVID-19 and the RAS. RESULTS: Several studies have indicated that the downregulation of membrane-bound ACE2 may exert a key role for the impairment of immune functions and for COVID-19 patients' outcomes. The downregulation may occur by distinct mechanisms, particularly: (1) the shedding process induced by the SARS-CoV-2 fusion pathway, which reduces the amount of membrane-bound ACE2, stimulating more shedding by the high levels of Angiotensin II; (2) the endocytosis of ACE2 receptor with the virus itself and (3) by the interferon inhibition caused by SARS-CoV-2 effects on the immune system, which leads to a reduction of ACE2 receptor expression. CONCLUSION: Recent research provides evidence of a reduction of the components of the alternative RAS axis, including ACE2 and Angiotensin-(1-7). In contrast, increased levels of Angiotensin II can activate the AT1 receptor in several organs. Consequently, increased inflammation, thrombosis and angiogenesis occur in patients infected with SARS-COV-2. Attention should be paid to the interactions of the RAS and COVID-19, mainly in the context of novel vaccines and proposed medications.
  • |*SARS-CoV-2[MESH]
  • |Angiotensin-Converting Enzyme 2/*genetics[MESH]
  • |Angiotensin-Converting Enzyme Inhibitors/pharmacology[MESH]
  • |Animals[MESH]
  • |Antiviral Agents/pharmacology[MESH]
  • |COVID-19 Drug Treatment[MESH]
  • |COVID-19/etiology/genetics/*immunology[MESH]
  • |Down-Regulation[MESH]
  • |Endocytosis/drug effects/immunology[MESH]
  • |Humans[MESH]
  • |Inflammation[MESH]
  • |Mice[MESH]
  • |Renin-Angiotensin System/drug effects/*immunology[MESH]
  • |Virus Internalization/drug effects[MESH]


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