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Table 1 Main mechanisms of oxidative-burden related COPD

From: Novel drug delivery systems targeting oxidative stress in chronic obstructive pulmonary disease: a review

Mechanism Outcome Refs.
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]
  1. iNOS, inducible nitric oxide synthase isoenzymes; SLPI, secretory leukocyte protease inhibitor; α1AT, alpha-1-antitrypsin; IL-1, interleukin 1; NF-κB, nuclear factor kappa B; IL-8, interleukin-8; GM-CSF, TNF-α, tumor necrosis factor-α; granulocyte macrophage colony-stimulating factor; iNOS, inducible nitric oxide synthase; HDAC: histone deacetylase