Cellular senescence limits acute lung injury induced by mechanical ventilation

Jorge Blazquez-Prieto; Covadonga Huidobro; Ines Lopez-Alonso; Laura Amado-Rodriguez; Paula Martin-Vicente; Cecilia Lopez-Martinez; Irene Crespo; Cristina Pantoja; Pablo J Fernandez-Marcos; Manuel Serrano; Jacob I Sznajder; Guillermo M Albaiceta

The lungs have a stereotypic response to acute injury, which is preserved among species and many etiological agents. Once damage is inflicted, lung cells trigger a host response which can include inflammation, matrix remodeling and different forms of cell death, including apoptosis (1) . Although a limited host response may help to clear the injurious agent and repair lung tissue (2) , an overexuberant host response can lead to severe injury and impairment in gas exchange. Therefore, therapeutic strategies aimed to limit lung damage and interference with lung repair are important. Lungs are exposed to mechanical load during every breath. In pathologic conditions, generation of the pressure gradients necessary for ventilation may cause an excessive cell stretch and lead to organ dysfunction. This is especially relevant during mechanical ventilation with high pressures, which can lead to the so-called ventilator-induced lung injury (VILI) (3, 4) . In mechanically ventilated patients , a strategy aimed to limit VILI decreased mortality in patients with the acute respiratory distress syndrome (ARDS) (5) .