Intensive care medicine

Cell biology

Biology

ARDS

Surgery

Fibrosis

Regeneration (biology)

Diffuse alveolar damage

Acute respiratory distress

Vascular permeability

Internal medicine

Pulmonary fibrosis

Medicine

Lung

Pulmonary edema

Pathology

CHEST Journal

ARDS is an acute inflammatory pulmonary process triggered by severe pulmonary and systemic insults to the alveolar-capillary membrane. This causes increased vascular permeability and the development of interstitial and alveolar protein-rich edema, leading to acute hypoxemic respiratory failure. Supportive treatment includes the use of lung-protective ventilatory strategies that decrease the work of breathing, can improve oxygenation, and minimize ventilator-induced lung injury. Despite substantial advances in supportive measures, there are no specific pharmacologic treatments for ARDS, and the overall hospital mortality rate remains about 40% in most series. The pathophysiology of ARDS involves interactions among multiple mechanisms, including immune cell infiltration, cytokine storm, alveolar-capillary barrier disruption, cell apoptosis, and the development of fibrosis. Here we review some new developments in the molecular basis of lung injury, with a focus on possible novel pharmacologic interventions aimed at improving the outcomes of patients with ARDS. Our focus is on platelet-endothelial cell adhesion molecule-1, which contributes to the maintenance and restoration of vascular integrity following barrier disruption. We also highlight the wingless-related integration site signaling pathway, which appears to be a central mechanism for lung healing as well as for fibrotic development. ARDS is an acute inflammatory pulmonary process triggered by severe pulmonary and systemic insults to the alveolar-capillary membrane. This causes increased vascular permeability and the development of interstitial and alveolar protein-rich edema, leading to acute hypoxemic respiratory failure. Supportive treatment includes the use of lung-protective ventilatory strategies that decrease the work of breathing, can improve oxygenation, and minimize ventilator-induced lung injury. Despite substantial advances in supportive measures, there are no specific pharmacologic treatments for ARDS, and the overall hospital mortality rate remains about 40% in most series. The pathophysiology of ARDS involves interactions among multiple mechanisms, including immune cell infiltration, cytokine storm, alveolar-capillary barrier disruption, cell apoptosis, and the development of fibrosis. Here we review some new developments in the molecular basis of lung injury, with a focus on possible novel pharmacologic interventions aimed at improving the outcomes of patients with ARDS. Our focus is on platelet-endothelial cell adhesion molecule-1, which contributes to the maintenance and restoration of vascular integrity following barrier disruption. We also highlight the wingless-related integration site signaling pathway, which appears to be a central mechanism for lung healing as well as for fibrotic development.

Lung Repair and Regeneration in ARDS