PPARGC1A and chronic obstructive pulmonary disease: In the lung tissue of patients with mild COPD, PGC1-α level was increased, which may be a compensatory mechanism that attempted to respond to initial oxidative stress and inflammatory damage by enhancing mitochondrial biogenesis; however, as the disease progresses to moderate-severe stages, PGC1-α levels progressively decreased, indicating that the mitochondrial biogenesis process was severely impaired (Li et al., 2010).