<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>272</volume><submitter>Chiappalupi S</submitter><funding>Associazione Italiana per la Ricerca sul Cancro</funding><funding>Fondazione Cassa di Risparmio di Perugia</funding><pubmed_abstract>A novel infectious disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was detected in December 2019 and declared as a global pandemic by the World Health. Approximately 15% of patients with COVID-19 progress to severe pneumonia and eventually develop acute respiratory distress syndrome (ARDS), septic shock and/or multiple organ failure with high morbidity and mortality. Evidence points towards a determinant pathogenic role of members of the renin-angiotensin system (RAS) in mediating the susceptibility, infection, inflammatory response and parenchymal injury in lungs and other organs of COVID-19 patients. The receptor for advanced glycation end-products (RAGE), a member of the immunoglobulin superfamily, has important roles in pulmonary pathological states, including fibrosis, pneumonia and ARDS. RAGE overexpression/hyperactivation is essential to the deleterious effects of RAS in several pathological processes, including hypertension, chronic kidney and cardiovascular diseases, and diabetes, all of which are major comorbidities of SARS-CoV-2 infection. We propose RAGE as an additional molecular target in COVID-19 patients for ameliorating the multi-organ pathology induced by the virus and improving survival, also in the perspective of future infections by other coronaviruses.</pubmed_abstract><journal>Life sciences</journal><pagination>119251</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7900755</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives.</pubmed_title><pmcid>PMC7900755</pmcid><pubmed_authors>Chiappalupi S</pubmed_authors><pubmed_authors>Salvadori L</pubmed_authors><pubmed_authors>Riuzzi F</pubmed_authors><pubmed_authors>Vukasinovic A</pubmed_authors><pubmed_authors>Sorci G</pubmed_authors><pubmed_authors>Donato R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives.</name><description>A novel infectious disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was detected in December 2019 and declared as a global pandemic by the World Health. Approximately 15% of patients with COVID-19 progress to severe pneumonia and eventually develop acute respiratory distress syndrome (ARDS), septic shock and/or multiple organ failure with high morbidity and mortality. Evidence points towards a determinant pathogenic role of members of the renin-angiotensin system (RAS) in mediating the susceptibility, infection, inflammatory response and parenchymal injury in lungs and other organs of COVID-19 patients. The receptor for advanced glycation end-products (RAGE), a member of the immunoglobulin superfamily, has important roles in pulmonary pathological states, including fibrosis, pneumonia and ARDS. RAGE overexpression/hyperactivation is essential to the deleterious effects of RAS in several pathological processes, including hypertension, chronic kidney and cardiovascular diseases, and diabetes, all of which are major comorbidities of SARS-CoV-2 infection. We propose RAGE as an additional molecular target in COVID-19 patients for ameliorating the multi-organ pathology induced by the virus and improving survival, also in the perspective of future infections by other coronaviruses.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 May</publication><modification>2024-12-04T06:48:38.35Z</modification><creation>2021-02-27T08:16:51Z</creation></dates><accession>S-EPMC7900755</accession><cross_references><pubmed>33636175</pubmed><doi>10.1016/j.lfs.2021.119251</doi></cross_references></HashMap>