In a study of idiopathic pulmonary fibrosis (IPF) subjects, researchers found that PGC-1α, which increases the enzymatic capacity for fatty acid oxidation (FAO) and abolishes glycolysis, was augmented in macrophages, whereas the effects of PGC-1α were diminished in a dominant-negative MCU model (57–59). Here, PPARGC1A is linked to pulmonary fibrosis.