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Pathogenesis of pulmonary emphysema - cellular and molecular events.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Petta, Antonio Di |
| Copyright Year | 2010 |
| 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. |
| Starting Page | 142 |
| Ending Page | 144 |
| Page Count | 3 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://www.scielo.br/pdf/eins/v8n2/pt_1679-4508-eins-8-2-0248.pdf |
| Alternate Webpage(s) | http://apps.einstein.br/revista/arquivos/PDF/1480-Einstein_v8n2_p248-51.pdf |
| PubMed reference number | 26760013v1 |
| Alternate Webpage(s) | https://doi.org/10.1590/S1679-45082010RB1480 |
| DOI | 10.1590/S1679-45082010RB1480 |
| Journal | Einstein |
| Volume Number | 8 |
| Issue Number | 2 |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Alveolar wall Apoptosis Bronchioles Cell Aging Chronic Obstructive Airway Disease Elastic Fibers Extracellular Matrix Hypertrophy Lung hyperinflation Oxidative Stress Protease Inhibitors Pulmonary Emphysema Structure of parenchyma of lung Wound Healing |
| Content Type | Text |
| Resource Type | Article |