[HTML][HTML] SARS-CoV-2-mediated inflammatory response in lungs: should we look at RAGE?

A Rojas, I Gonzalez, MA Morales - Inflammation Research, 2020 - Springer
Inflammation Research, 2020Springer
In December 2019, a new type of coronavirus pneumonia (COVID-19) emerged in Wuhan,
China, and spread rapidly all over the world, forcing the World Health Organization to
officially declare on 30 January 2020, the COVID-19 as a global pandemic. Lung
inflammation is the main cause of life-threatening respiratory disorders at the COVID-19
severe stage [1, 2]. The etiological agent of this new pandemic is a novel coronavirus, the
SARS-CoV2, which uses the angiotensin converting enzyme 2 (ACE2) molecule as the …
In December 2019, a new type of coronavirus pneumonia (COVID-19) emerged in Wuhan, China, and spread rapidly all over the world, forcing the World Health Organization to officially declare on 30 January 2020, the COVID-19 as a global pandemic. Lung inflammation is the main cause of life-threatening respiratory disorders at the COVID-19 severe stage [1, 2].
The etiological agent of this new pandemic is a novel coronavirus, the SARS-CoV2, which uses the angiotensin converting enzyme 2 (ACE2) molecule as the receptor for viral cell entry [3]. ACE2 plays an important role in the renin–angiotensin system (RAS), and the imbalance between ACE/Ang II/AT1R pathway and ACE2/Ang (1–7)/Mas receptor pathway in the RAS system will lead to multisystem inflammation [4].
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