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Am J Physiol Lung Cell Mol Physiol . Metabolic signatures of acute respiratory distress syndrome: COVID VS non-COVID

tetano

Editor, Senior Moderator
Am J Physiol Lung Cell Mol Physiol


. 2024 Mar 12.
doi: 10.1152/ajplung.00266.2023. Online ahead of print. Metabolic signatures of acute respiratory distress syndrome: COVID VS non-COVID

Xiangming Ji[SUP] 1 [/SUP], Hong-Long Ji[SUP] 2 [/SUP]



Affiliations
Abstract

Acute respiratory distress syndrome (ARDS) is a fatal pulmonary disorder characterized by severe hypoxia and inflammation. Systemic and pulmonary infections are a leading cause of ARDS. The common respiratory pathogens include bacteria and virus, including Pseudomonas aeruginosa, Streptococcus aureus, Enterobacter species, coronavirus, influenza, and herpesviruses. COVID-19-associated ARDS is a new etiologic phenotype of the disease. The pathogenesis of ARDS caused by bacteria and viruses differs in host immune responses and lung mesenchymal injury. We postulate that both systemic and lung metabolomics of ARDS induced by virus may differ from those infected by other pathogens. This review aims to compare the metabolic signatures in blood and lung specimens. Both common and SARS-CoV-2-specific metabolomic signatures were comprehensively reviewed. The differences in metabolic profiles between COVID-19 and other etiology-associated ARDS may uncover new biomarkers, pathogenic mechanisms, druggable targets, and differential diagnosis.

Keywords: Acute respiratory distress syndrome (ARDS); COVID-19; lipidomics; metabolomics.

 
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