Emphysema Research Paper

Emphysema belongs to chronic obstructive pulmonary disease (COPD). It is characterized by permanent airflow restriction resulting from a unique pattern of alveolar wall destruction, enlargement of alveolar airspace and loss of lung structure and elasticity. Cigarette smoke is a main risk factor of this disease development [1]. However, the pathophysiology of emphysema is not fully understood [2]. This disease is associated with an increased oxidative stress (REF), which may cause DNA damage. Under normal conditions, the level of reactive oxygen species (ROS) in the cell is controlled by antioxidant defense systems, which prevent damage of nucleic acids and proteins. However, the impairment or imbalance between oxidants and antioxidants in the …show more content…
They are the most harmful forms of DNA damage. DSBs may lead to programmed cell death, thereby eliminating cells with potentially harmful mutations or activation of DNA repair mechanisms to eliminate DNA damage. Cells cannot survive with even one unrepaired DSB, which indicates the importance of the functional DNA damage repair system [6]. Two key and separate mechanisms are involved in DSBs repair: non-homologous end-joining (NHEJ) and homologous recombination (HR) [7]. Their selective activation depends on the cell cycle and nature of the factor(s), which induced DSBs. HR is considered as the most accurate system of DSBs repair and is essential for the maintenance of chromosomal integrity [7, 8]. However, it has been reported that NHEJ is likely playing the largest role in DSBs repair in humans, is also a faster and more efficient pathway than HR (add this REF Comparison of nonhomologous end joining and homologous recombination in human cells, Zhiyong Mao, Michael Bozzella, Andrei Seluanov, and Vera Gorbunova). Moreover, the NHEJ is also essential for V(D)J recombination during T- and B-cell lymphocyte development (Davis AJ, Chen DJ, 2013 – Transl Cancer Res). The NHEJ repair pathway includes Ku70, Ku86, DNA ligase IV, XRCC4 (X-ray repair cross-complementing protein 4), Artemis, XLF (XRCC4-like factor) and DNA-PKcs (DNA-dependent protein kinase, catalytic subunit). Induction of this system

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