Pathogenesis of pulmonary emphysema – cellular and molecular events

Abstract

Pulmonary emphysema is a chronic obstructive disease, resulting from important alterations in the whole distal structure of terminal bronchioles, either by enlargement of air spaces or by destruction of the alveolar wall, leading to loss of respiratory surface, decreased elastic recoil and lung hyperinflation. For many years, the hypothesis of protease-antiprotease unbalance prevailed as the central theme in the pathogenesis of pulmonary emphysema. According to this hypothesis, the release of active proteolytic enzymes, produced mainly by neutrophils and macrophages, degrades the extracellular matrix, affecting the integrity of its components, especially collagen and elastic fibers. However, new concepts involving cellular and molecular events were proposed, including oxidative stress, cell apoptosis, cellular senescence and failed lung tissue repair. The aim of this review paper was to evaluate the cellular and molecular mechanisms seen in the pathogenesis of pulmonary emphysema.

Major clinical application of adipose derived stem cells

“…Clinically present as inflammation of the air tubes called Bronchitis and increased mucous production resulting in airway obstruction. Histologically the obstruction is caused by activated inflammatory cells which produce bronchiolar breakdown of the structural proteins (collagen and elastin) along with cellular apoptosis, inappropriate production of Matrix Metalloproteinase-9 (MMP9) and lack of lung tissue repair function [51,52] . In a small group of cases there is enlargement of lung spaces with fibrosis and narrowing of bronchioles resulting in emphysema.…”