Evaluation of Mitochondrial Dysfunction Factors in the Lungs of Patients with COPD

Chronic Obstructive Pulmonary Disease (COPD) is the third deadliest disease in the world and is spreading in developed countries. In 2011, the number of patients with COPD in the United States was estimated at 15 million, this population is expected to be increasing. COPD is usually associated with an increase in reactive oxygen species (ROS) and emphysema in lung cells that this rising is also due to impaired mitochondrial division and fusion, impaired mitophagia, loss of balance between oxidant / antioxidant enzymes, proteolytic / antiproteolytic, and epigenetic changes that ultimately leads to premature aging of lung cells. The balance between oxidant / antioxidant enzymes is one of the factors that control the release of ROS, increasing the expression of TGF-β disturbs this balance. One of the causes of COPD is cigarette smoke, which leads to cellular aging by disrupting the mitophage process. One of the epigenetic factors of this disease are the toxicity of histones in these people, which leads to mitochondrial toxicity. The common point of all these pathways is mitochondrial dysfunction. Mitochondria are dynamic organelle with fusion and intracellular division. Mitochondrial division is associated with apoptosis and mitophagy (selective destruction of damaged mitochondria), while mitochondrial fusion has the opposite role. It seems that research on mitochondrial organelles can increase our knowledge about COPD and can help identify the cellular and molecular pathways of the disease.