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Review
. 2020 May 28:15:3803-3826.
doi: 10.2147/IJN.S242516. eCollection 2020.

Conventional and Nanotechnology Based Approaches to Combat Chronic Obstructive Pulmonary Disease: Implications for Chronic Airway Diseases

Affiliations
Review

Conventional and Nanotechnology Based Approaches to Combat Chronic Obstructive Pulmonary Disease: Implications for Chronic Airway Diseases

Mehak Passi et al. Int J Nanomedicine. .

Abstract

Chronic obstructive pulmonary disease (COPD) is the most prevalent obstructive lung disease worldwide characterized by decline in lung function. It is associated with airway obstruction, oxidative stress, chronic inflammation, mucus hypersecretion, and enhanced autophagy and cellular senescence. Cigarette smoke being the major risk factor, other secondary risk factors such as the exposure to air pollutants, occupational exposure to gases and fumes in developing countries, also contribute to the pathogenesis of COPD. Conventional therapeutic strategies of COPD are based on anti-oxidant and anti-inflammatory drugs. However, traditional anti-oxidant pharmacological therapies are commonly used to alleviate the impact of COPD as they have many associated repercussions such as low diffusion rate and inappropriate drug pharmacokinetics. Recent advances in nanotechnology and stem cell research have shed new light on the current treatment of chronic airway disease. This review is focused on some of the anti-oxidant therapies currently used in the treatment and management of COPD with more emphasis on the recent advances in nanotechnology-based therapeutics including stem cell and gene therapy approaches for the treatment of chronic airway disease such as COPD and asthma.

Keywords: COPD; anti-oxidant therapy; chronic obstructive pulmonary disease; gene therapy; nanotechnology; stem cell therapy.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
Factors that influence the pathogenesis of COPD.
Figure 2
Figure 2
Mode of action of NAC and GSH synthesis.
Figure 3
Figure 3
Nrf2 mechanism of action. Oxidative stress resulting from cigarette smoke, reactive oxygen species (ROS), particulate matter etc. leads to dissociation of Keap1-Nrf2 followed by its stabilization and nuclear translocation, where it upregulates the various antioxidant genes that protect the body. In COPD, there is an increased Nrf2 proteasomal degradation as a result of increased Keap1 production and reduction in master stabilization DJ-1 protein.
Figure 4
Figure 4
Schematic representation of the EPR Effect.
Figure 5
Figure 5
Various nanocarriers for drug delivery to the lungs.
Figure 6
Figure 6
Liposomal nanocarriers, Copyright 2015, American Chemical Society.
Figure 7
Figure 7
Pyrrolidiniumdendriplexes Copyright 2017, American Chemical Society.
Figure 8
Figure 8
Nano-in microparticles (NIMs) containing superparamagnetic iron oxide nanoparticles (SPIONs) Copyright 2017, American Chemical Society.
Figure 9
Figure 9
Assessments of fluorescently encoded poly(vinyl alcohol) (PVA)-coated gold nanoparticles using a 3D co-culture model consisting of epithelial and immune cells (macrophages and dendritic cells). Copyright 2016, American Chemical Society.
Figure 10
Figure 10
Liposomal-based theranostic nanoparticles. Copyright 2011, American Chemical Society.

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