Fig. 5From: Failed upregulation of TFAM protein and mitochondrial DNA in oxidatively deficient fibers of chronic obstructive pulmonary disease locomotor muscleMarkers of mitochondrial biogenesis and oxidative metabolism in vastus lateralis muscle homogenates of COPD patients relative to controls. a Higher levels of mitochondrial biogenesis and oxidative metabolism markers in COPD (two-way ANOVA revealed the significant main effect of disease status, P < 0.01; TFAM and PGC-1α; COPD n = 17, controls n = 11, NRF1, PGC1β, PPAR δ, and PPAR γ; COPD n = 9 controls n = 9). b Significant correlation between upregulated mitochondrial biogenesis signals PGC-1α and TFAM in COPD patients (r 2 = 0.99, n = 10; P < 0.001). c Levels of TFAM protein in COPD patients (0.76 ± 0.14, n = 20) and control subjects (1.0 ± 0.23, n = 10; P = 0.18) assessed by Western blot. d Lower ratio of TFAM protein relative to TFAM mRNA in COPD patients (0.25 ± 0.07) compared to controls (0.94 ± 0.2; *P < 0.5). e Lower levels of citric synthase activity in COPD patients (4.62 ± 0.33, n = 19) than controls (13.44 ± 1.14, n = 14; ***P < 0.001). f Positive relationship between TFAM and CS exists in controls (r 2 = 0.67, P < 0.1) but not in COPD patients (r 2 < 0.1). Measured levels of CS activity in COPD are 51 % lower than predicted for the measured TFAM protein. Graphs show mean ± SEMBack to article page