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Licence to kill senescent cells in idiopathic pulmonary fibrosis?

2017; European Respiratory Society; Volume: 50; Issue: 2 Linguagem: Inglês

10.1183/13993003.01360-2017

1399-3003

Arnaud Mailleux, Bruno Crestani,

Medical Imaging and Pathology Studies

Idiopathic pulmonary fibrosis (IPF) is a rare chronic fibrotic pulmonary disease of unknown aetiology, which results in the progressive destruction of lung with a very poor median survival of 3 years after diagnosis. According to the current paradigm, IPF results from progressive alterations of alveolar epithelial cells leading to the recruitment of mesenchymal cells to the alveolar regions of the lung with secondary deposition of extracellular matrix, and destruction of the normal lung structure and physiology [1]. The anarchic epithelial repair observed in IPF is also accompanied by reactivation of signalling pathways involved in fetal lung development [2]. IPF develops in a genetically susceptible individual, and is promoted by interaction with environmental agents such as inhaled particles, tobacco smoke, inhaled pollutants, and viral and bacterial agents. Two drugs are currently available for the treatment of pulmonary fibrosis: pirfenidone, a small molecule that probably targets lung fibroblasts through multiple mechanisms; and nintedanib, a multitarget tyrosine kinase inhibitor [1]. Targeting senescent cells may prove useful in the future treatment of idiopathic pulmonary fibrosis