Table 2.
Metabolic reprogramming in chronic lung diseases
| Cell process | BPD | COPD | Lung Fibrosis |
|---|---|---|---|
| Glycolysis | Hyperoxia increased glucose uptake but reduced glycolytic capacity and reserve in MLE-12 (23). | Cigarette smoke reduced glycolysis in type II cells (1). | Increased glycolysis during lung fibrosis (20, 35, 99) |
| PPP | Hyperoxia increased PPP in lipofibroblasts (15). | Compensatory increase in PPP (2) | Trend in increased PPP |
| Mitochondrial respiration | Reduced mitochondrial respiration in BPD and hyperoxia-exposed MLE-12 cells (23, 51) | Disrupted lipid metabolism (5, 57, 69, 86, 91) | Reduced mitochondrial respiration during lung fibrosis (105) |
| FA oxidation | FABP4 and FABP5 were increased (34). | Cigarette smoke enhances FA uptake and oxidation (1). | Reduced FA oxidation (105) |
| Amino acid metabolism | L-type amino acid transporter-1 was reduced BPD patients (12). | Increased glutamine, serine, histidine, arginine, proline, asparagine, aspartic acid, glycine-proline and lysine in patients with emphysema (87) | Increased serine, glycine, and proline synthesis (13) |
| Metabolite | Urine lactate was increased in BPD patients (33). | Acetyl CoA, succinate, NADH, and FADH2 reduction in smokers (27) | Overall reduction of TCA cycle metabolites and enzymes (105) |
BPD, bronchopulmonary dysplasia; COPD, chronic obstructive pulmonary disease.