tetano
Editor, Senior Moderator
Life Sci
. 2021 Feb 23;272:119251.
doi: 10.1016/j.lfs.2021.119251. Online ahead of print.
Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives
Sara Chiappalupi[SUP] 1 [/SUP], Laura Salvadori[SUP] 2 [/SUP], Aleksandra Vukasinovic[SUP] 1 [/SUP], Rosario Donato[SUP] 3 [/SUP], Guglielmo Sorci[SUP] 4 [/SUP], Francesca Riuzzi[SUP] 5 [/SUP]
Affiliations
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.
Keywords: COVID-19; HMGB1; RAGE; Renin-angiotensin system (RAS); SARS-CoV-2.
. 2021 Feb 23;272:119251.
doi: 10.1016/j.lfs.2021.119251. Online ahead of print.
Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives
Sara Chiappalupi[SUP] 1 [/SUP], Laura Salvadori[SUP] 2 [/SUP], Aleksandra Vukasinovic[SUP] 1 [/SUP], Rosario Donato[SUP] 3 [/SUP], Guglielmo Sorci[SUP] 4 [/SUP], Francesca Riuzzi[SUP] 5 [/SUP]
Affiliations
- PMID: 33636175
- PMCID: PMC7900755
- DOI: 10.1016/j.lfs.2021.119251
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.
Keywords: COVID-19; HMGB1; RAGE; Renin-angiotensin system (RAS); SARS-CoV-2.