UCP2 and pulmonary fibrosis: Although it appears counter-intuitive that the absence of a H2O2-generating system (i.e. NOX4) leads to an antioxidant response, a recent study showed that increased UCP2 in lung fibroblasts of idiopathic pulmonary fibrosis has a profibrotic impact associated with increased oxidative stress, impaired ATP synthesis and senescence [91].