Article Review
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Article Review
According to Yao and Rahman (2011), the management options for chronic obstructive pulmonary disease (COPD) are very limited and the mainstay is dilators of the bronchus. It is alarming because the disease burden for COPD is much higher. This article focuses on the etiology of the disease and it is stated that the main factor that incites the pathology that leads to COPD is strongly dependent on the stress and inflammation. It is made clear in the article that this disease is multifactorial. Cigarette smoking increases the quantity of free radicals which causes imbalance between oxidants and anti-oxidants. This causes a responsive increase in transcription factors like NF-κB. These transcription factors cause autophagy and abnormal protein unfolding response. The manifestations of oxidative injury to the lungs in COPD spans around:
Increased quantity of exogenous and endogenous reactive oxygen species (ROS)
Oxidative stress mediated neurogenic lung inflammation
Oxidative stress induced cellular autophagy and apoptosis
Oxidative stress induced increment in unfolded protein response (UPR)
In a more recent discovery, it has been postulated and proved that there is a strong predilection for epigenetic development in the development of COPD.
Similarly, in an another study conducted by Adenuga et al. (2009), patients with a history of long standing smoking are prone to develop COPD and other respiratory pathology because they are increase the oxidative stress load in the body. In another study conducted by Andre et al. (2008), it was proved that cigarette smoking causes abnormal inflammation of the airways that leads to expression of certain self-destructing receptors and factors.
It is, therefore, proven on different occasions that smoking is the most important cause of COPD. The pathology manifests through various modes and morphology, but eventually it causes COPD. Learning of pathogenesis of COPD in greater depth gives an insight which aids in preparing, choosing and administering the right medication.
References
Adenuga, D., Yao, H., March, T. H., Seagrave, J., & Rahman, I. (2009). Histone Deacetylase 2 Is Phosphorylated, Ubiquitinated, and Degraded by Cigarette Smoke. American Journal of Respiratory Cell and Molecular Biology,40(4), 464–473. http://doi.org/10.1165/rcmb.2008-0255OC
Andrè, E., Campi, B., Materazzi, S., Trevisani, M., Amadesi, S., Massi, D., Patacchini, R. (2008). Cigarette smoke–induced neurogenic inflammation is mediated by α,β-unsaturated aldehydes and the TRPA1 receptor in rodents.The Journal of Clinical Investigation, 118(7), 2574–2582. http://doi.org/10.1172/JCI34886
Yao, H., & Rahman, I. (2011). Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease. Toxicology and Applied Pharmacology, 254(2), 72–85. http://doi.org/10.1016/j.taap.2009.10.022
