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dc.contributor.author
Goldin, Carla Jimena
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dc.contributor.author
Vázquez, Ramiro José
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dc.contributor.author
Polack, Fernando Pedro
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dc.contributor.author
Álvarez Paggi, Damián Jorge
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dc.date.available
2020-10-13T17:18:30Z
dc.date.issued
2020-09
dc.identifier.citation
Goldin, Carla Jimena; Vázquez, Ramiro José; Polack, Fernando Pedro; Álvarez Paggi, Damián Jorge; Identifying pathophysiological bases of disease in COVID-19; BioMed Central; Translational Medicine Communications; 5; 1; 9-2020; 1-12
dc.identifier.uri
http://hdl.handle.net/11336/115800
dc.description.abstract
COVID-19 is an infectious disease caused by the SARS-CoV-2 virus that can affect lung physiology encompassing a wide spectrum of severities, ranging from asymptomatic and mild symptoms to severe and fatal cases; the latter including massive neutrophil infiltration, stroke and multiple organ failure. Despite many recents findings, a clear mechanistic description underlying symptomatology is lacking. In this article, we thoroughly review the available data involving risk factors, age, gender, comorbidities, symptoms of disease, cellular and molecular mechanisms and the details behind host/pathogen interaction that hints at the existence of different pathophysiological mechanisms of disease. There is clear evidence that, by targeting the angiotensin-converting enzyme II (ACE2) –its natural receptor–, SARS-CoV-2 would mainly affect the reninangiotensin-aldosterone system (RAAS), whose imbalance triggers diverse symptomatology-associated pathological processes. Downstream actors of the RAAS cascade are identified, and their interaction with risk factors and comorbidities are presented, rationalizing why a specific subgroup of individuals that present already lower ACE2 levels is particularly more susceptible to severe forms of disease. Finally, the notion of endotype discovery in the context of COVID-19 is introduced. We hypothesize that COVID-19, and its associated spectrum of severities, is an umbrella term covering different pathophysiological mechanisms (endotypes). This approach should dramatically accelerate our understanding and treatment of disease(s), enabling further discovery of pathophysiological mechanisms and leading to the identification of specific groups of patients that may benefit from personalized treatments.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
BioMed Central
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
SARS-COV-2
dc.subject
COVID-19
dc.subject
ENDOTYPES
dc.subject
PATHOPHYSIOLOGY
dc.subject.classification
Inmunología
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Identifying pathophysiological bases of disease in COVID-19
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-10-13T15:57:42Z
dc.identifier.eissn
2396-832X
dc.journal.volume
5
dc.journal.number
1
dc.journal.pagination
1-12
dc.journal.pais
Reino Unido
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dc.journal.ciudad
Londres
dc.description.fil
Fil: Goldin, Carla Jimena. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Vázquez, Ramiro José. Fondazione Istituto Italiano di Tecnologia; Italia. Early Drug Development Group; Francia
dc.description.fil
Fil: Polack, Fernando Pedro. Fundación para la Investigación en Infectología Infantil; Argentina
dc.description.fil
Fil: Álvarez Paggi, Damián Jorge. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.journal.title
Translational Medicine Communications
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://transmedcomms.biomedcentral.com/articles/10.1186/s41231-020-00067-w
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1186/s41231-020-00067-w
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