How a fibroblast ages: a role for bone morphogenetic protein 4 in protecting lung fibroblasts from senescence in pulmonary fibrosis

Idiopathic pulmonary fibrosis (IPF) is a deadly lung parenchymal disease that causes progressive scarring, functional deterioration and death [1]. Current treatments are inadequate, since they are incapable of reversing the progression of disease. Transforming growth factor-β (TGF-β) has emerged as a significant cause of fibrosis due to its stimulation of fibroblast differentiation and activation, as well as related pro-fibrotic characteristics such as apoptosis resistance, metabolic reprogramming and senescence [2]. Despite its critical importance, targeting of TGF-β has proven difficult due to its broad biological roles in immune regulation and tumour suppression, as well as tissue and vascular development and maintenance, as demonstrated in SMAD3 knockout mice [3]. This editorial summarises the findings of an article showing a role for bone morphogenetic protein 4 in protecting fibroblasts from senescence and pulmonary fibrosis and puts them into the context of the current literature https://bit.ly/3rrHZ0y