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SARS-CoV-2-mediated inflammatory response in lungs: should we look at rage?
dc.contributor.author | Rojas, Armando | |
dc.contributor.author | González-Bonet, Ileana | |
dc.contributor.author | Morales, Miguel A. | |
dc.date.accessioned | 2020-09-09T19:20:10Z | |
dc.date.available | 2020-09-09T19:20:10Z | |
dc.date.issued | 2020 | |
dc.identifier.uri | http://repositorio.ucm.cl/handle/ucm/3059 | |
dc.description.abstract | The novel coronavirus disease (COVID-19) pandemic is placing significant strains on health systems, scientific communities, essential public services, and economies all over the world. In this context, the world´s scientific biomedical establishment is unleashing an unprecedented response to the COVID-19 pandemic. This is a battle against time, considering the thousands of human lives are lost every day. In this commentary, based on a very recent research report, we intend to highlight how a new mechanism describing the RAGE transactivation produced by Ang II-mediated ATR1 activation can run continuously and thus, reinforcing a sustained inflammation in lungs, due to the SARS-Cov-2-mediated imbalance of the ACE/And II/ATR1 pathway. | es_CL |
dc.language.iso | en | es_CL |
dc.rights | Atribución-NoComercial-SinDerivadas 3.0 Chile | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | * |
dc.source | Inflammation Research, 69(7), 1-3 | es_CL |
dc.subject | Receptor of advanced glycation end-products | es_CL |
dc.subject | SARS-CoV-2 | es_CL |
dc.subject | Inflammation | es_CL |
dc.subject | Lungs | es_CL |
dc.subject | Receptor transactivation | es_CL |
dc.subject | Angiotensin II | es_CL |
dc.title | SARS-CoV-2-mediated inflammatory response in lungs: should we look at rage? | es_CL |
dc.type | Article | es_CL |
dc.ucm.facultad | Facultad de Medicina | es_CL |
dc.ucm.indexacion | Scopus | es_CL |
dc.ucm.indexacion | Isi | es_CL |
dc.ucm.uri | link.springer.com/article/10.1007/s00011-020-01353-x | es_CL |
dc.ucm.doi | doi.org/10.1007/s00011-020-01353-x | es_CL |
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