Reprogramming of cellular metabolism: driver for airway remodelling in COPD?

Mitochondrial dysfunction, in particular decreased oxidative phosphorylation and increased production of mitochondrial reactive oxidant species (ROS), and changes in cellular metabolism are increasingly recognised as important events in the pathogenesis of a range of lung diseases, including asthma, chronic obstructive pulmonary disease (COPD), pulmonary arterial hypertension and lung cancer [1, 2]. We are beginning to understand how dysfunction of the mitochondria is linked to the altered use of metabolic pathways and how this impacts cellular function. This switch in use of different metabolic pathways is often referred to as metabolic reprogramming, repatterning or rewiring. Mitochondrial dysfunction and metabolic reprogramming are important for understanding cancer, immunity and inflammation, but studies focused on tissue remodelling have also revealed a regulatory role of these mechanisms [1, 2]. Mitochondrial dysfunction and metabolic changes contribute to inflammation and tissue remodelling in COPD <http://ow.ly/hgsm30gARnv>