The Pathogenesis Of COPD Hypothesis

Unfortunately, research progress in this field has been slow. Most basic scientific research over the past 35 years has focused on the pathogenetic roles of cigarette smoke, inflammation, and protease/antiprotease balance, based on the association of COPD with cigarette smoking and the early discovery that a subgroup of patients with emphysema is genetically deficient in an inhibitor of a neutrophil protease. Although the cigarette-inflammation-protease theory captures key features of COPD epidemiology and pathology, this approach has not yet led to a reduction in COPD prevalence or morbidity, to the development of any therapy proven to modify the disease process itself, or to an adequate understanding of how risk factors other than cigarette smoking may contribute to COPD pathogenesis.
Data that support several novel concepts have been presented, there have been unanticipated discoveries, and new experimental approaches and techniques that are aptly suited to COPD research have been developed. Furthermore, elucidation of cellular pathways that are critically involved in COPD pathogenesis may lead rapidly to clinical trials of potential therapeutics, given the improving capabilities of the pharmaceutical industry for development of mechanism-specific drugs. In conclusion, COPD is a condition in which there is limited air flow. It is caused by long term exposure to irritating gases or particulate matter, most often the form is cigarette smoke. COPD is treatable with the proper care and management, most people can achieve good symptom control and have a better outlook on quality of