• Jesús Villar, Haibo Zhang, and Arthur S Slutsky.
• CIBER de Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain; Multidisciplinary Organ Dysfunction Evaluation Research Network, Research Unit, Hospital Universitario Dr Negrin, Las Palmas de Gran Canaria, Spain; Keenan Research Center for Biomedical Sciences at the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Canada.
• Chest. 2019 Mar 1; 155 (3): 587-594.

AbstractARDS 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.Copyright © 2018 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

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