Acute respiratory distress syndrome (ARDS) remains a leading cause of morbidity and mortality in critically ill patients despite advances in supportive care and lung-protective ventilation. The syndrome is characterized by biological heterogeneity involving epithelial and endothelial injury, dysregulated inflammation, surfactant dysfunction, and impaired alveolar–capillary barrier integrity. This review integrates experimental, translational, and clinical evidence to examine the biological and molecular basis underlying ARDS, with particular emphasis on alveolar–capillary architecture, immune dysregulation, pulmonary mechanics, and the temporal evolution of diffuse alveolar damage. We further discuss emerging concepts in ARDS phenotyping and biomarker-based stratification as tools to address therapeutic heterogeneity and improve prognostic precision. Collectively, the evidence supports a shift from syndromic management toward biologically informed, precision-based approaches that may enable targeted interventions and improved clinical outcomes in ARDS.
Gonzalez-Plascencia et al. (Fri,) studied this question.