| http://purl.uniprot.org/citations/37966617 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/37966617 | http://www.w3.org/2000/01/rdf-schema#comment | "Acute respiratory distress syndrome (ARDS) is a common cause of hypoxemic respiratory failure in intensive care units that has increased dramatically as a result of the COVID-19 pandemic. In both COVID-19 and non-COVID ARDS, the pathogenesis of lung injury involves local (pulmonary) and systemic inflammation, leading to impaired gas exchange, requirement for mechanical ventilation, and a high risk of mortality. Heat shock protein 27 (HSP27) is a chaperone protein expressed in times of cell stress with roles in modulation of systemic inflammation via the NF-κB pathway. Given its important role as a modulator of inflammation, we sought to investigate the role of HSP27 and its associated auto-antibodies in ARDS caused by both SARS-CoV-2 and non-COVID etiologies. A total of 68 patients admitted to the intensive care unit with ARDS requiring mechanical ventilation were enrolled in a prospective, observational study that included 22 non-COVID-19 and 46 COVID-19 patients. Blood plasma levels of HSP27, anti-HSP27 auto-antibody (AAB), and cytokine profiles were measured on days 1 and 3 of ICU admission along with clinical outcome measures. Patients with COVID-19 ARDS displayed significantly higher levels of HSP27 in plasma, and a higher ratio of HSP27:AAB on both day 1 and day 3 of ICU admission. In patients with COVID-19, higher levels of circulating HSP27 and HSP27:AAB ratio were associated with a more severe systemic inflammatory response and adverse clinical outcomes including more severe hypoxemic respiratory failure. These findings implicate HSP27 as a marker of advanced pathogenesis of disease contributing to the dysregulated systemic inflammation and worse clinical outcomes in COVID-19 ARDS, and therefore may represent a potential therapeutic target."xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.org/dc/terms/identifier | "doi:10.1007/s12192-023-01381-6"xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/author | "Deng J."xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/author | "Chiu M.H."xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/author | "McDonald B."xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/author | "O'Brien E.R."xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/author | "Yu I.L."xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/author | "Gershkovich B."xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/name | "Cell Stress Chaperones"xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/pages | "877-887"xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/title | "Heat shock protein 27 in the pathogenesis of COVID-19 and non-COVID acute respiratory distress syndrome."xsd:string |
| http://purl.uniprot.org/citations/37966617 | http://purl.uniprot.org/core/volume | "28"xsd:string |
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