Alpha‐1‐antitrypsin : a possible host protective factor against Covid‐19

Loyola, Mariana Braccialli de; Reis, Thaís Tereza Aguiar dos; Oliveira, Guilherme Xavier Lyra Malcher de; Palmeira, Julys da Fonseca; Argañaraz, Gustavo Adolfo; Argañaraz, Enrique Roberto

Affichage complet

Élément Dublin Core	Valeur	Langue
dc.contributor.author	Loyola, Mariana Braccialli de	-
dc.contributor.author	Reis, Thaís Tereza Aguiar dos	-
dc.contributor.author	Oliveira, Guilherme Xavier Lyra Malcher de	-
dc.contributor.author	Palmeira, Julys da Fonseca	-
dc.contributor.author	Argañaraz, Gustavo Adolfo	-
dc.contributor.author	Argañaraz, Enrique Roberto	-
dc.date.accessioned	2021-01-18T13:39:23Z	-
dc.date.available	2021-01-18T13:39:23Z	-
dc.date.issued	2020-08-26	-
dc.identifier.citation	LOYOLA, Mariana Braccialli de et al. Alpha‐1‐antitrypsin: a possible host protective factor against Covid‐19. Reviews in Medical Virology, e2157, 2020. DOI: https://doi.org/10.1002/rmv.2157. Disponível em: https://onlinelibrary.wiley.com/doi/full/10.1002/rmv.2157.	pt_BR
dc.identifier.uri	https://repositorio.unb.br/handle/10482/39924	-
dc.language.iso	Inglês	pt_BR
dc.publisher	Wiley	pt_BR
dc.rights	Acesso Aberto	pt_BR
dc.title	Alpha‐1‐antitrypsin : a possible host protective factor against Covid‐19	pt_BR
dc.type	Artigo	pt_BR
dc.subject.keyword	A1AT	pt_BR
dc.subject.keyword	ADAM17	pt_BR
dc.subject.keyword	Covid-19	pt_BR
dc.subject.keyword	SARS-CoV-2	pt_BR
dc.subject.keyword	TMPRSS2	pt_BR
dc.identifier.doi	https://doi.org/10.1002/rmv.2157	pt_BR
dc.relation.publisherversion	https://onlinelibrary.wiley.com/doi/full/10.1002/rmv.2157	pt_BR
dc.description.abstract1	Understanding Covid‐19 pathophysiology is crucial for a better understanding of the disease and development of more effective treatments. Alpha‐1‐antitrypsin (A1AT) is a constitutive tissue protector with antiviral and anti‐inflammatory properties. A1AT inhibits SARS‐CoV‐2 infection and two of the most important proteases in the pathophysiology of Covid‐19: the transmembrane serine protease 2 (TMPRSS2) and the disintegrin and metalloproteinase 17 (ADAM17). It also inhibits the activity of inflammatory molecules, such as IL‐8, TNF‐α, and neutrophil elastase (NE). TMPRSS2 is essential for SARS‐CoV‐2‐S protein priming and viral infection. ADAM17 mediates ACE2, IL‐6R, and TNF‐α shedding. ACE2 is the SARS‐CoV‐2 entry receptor and a key component for the balance of the renin‐angiotensin system, inflammation, vascular permeability, and pulmonary homeostasis. In addition, clinical findings indicate that A1AT levels might be important in defining Covid‐19 outcomes, potentially partially explaining associations with air pollution and with diabetes. In this review, we focused on the interplay between A1AT with TMPRSS2, ADAM17 and immune molecules, and the role of A1AT in the pathophysiology of Covid‐19, opening new avenues for investigating effective treatments.	pt_BR
dc.identifier.orcid	https://orcid.org/0000-0002-7816-764X	pt_BR
dc.identifier.orcid	https://orcid.org/0000-0002-4359-7594	pt_BR
Collection(s) :	Artigos publicados em periódicos e afins UnB - Covid-19