As mitochondrial damage is related to NLRP3 activation through mitochondrial reactive oxygen species (mtROS) and oxidized mitochondrial DNA (mtDNA), which are increased in airway macrophages in cases of pulmonary fibrosis [99], we searched for colocalization of NC with proteins that are commonly recruited or present in mitochondria, including prohibitin (PHB) and PGC1α [5, 89]. This evidence concerns the gene PPARGC1A and pulmonary fibrosis.