Table 1 Main mechanisms of oxidative-burden related COPD

Imbalance of biological molecules

Reduced antioxidant and antiprotease enzyme activity (SOD, CAT, GPx, α1 antitrypsin);

Altered expression of ROS-related enzymes (decreased in CAT, GPx, SOD, and increase in iNOS);

Activation of metallo proteinases

[45,46,47,48,49]

Intracellular signaling

Altered expression of ROS related enzymes (decreased in CAT, GPx, SOD, and increase in iNOS)

[50, 51]

Mitochondrial respiration

Altered mitochondrial function

[46, 48, 52, 53]

Upregulation of gene transcription (NF-κB and, AP-1) and increase in cellular cytokine production

Increased gene expression of inflammatory mediators and cytokines (IL-1, TNF-α, IL-8, GM-CSF, iNOS)

[54]

Nuclear histone acetylation/deacetylation balance

Decreased HDAC2 activity and protein expression chronic inflammation (chronic remodelling)

[55, 56]

Remodelling of DNA/chromatin

Decreased histone deacetylase 2

[57]