Abstract

COPD: A SYSTEMATIC REVIEW

P. Thirupathy Kumaresan*, M. Kiruba, T. Shrinhidhi, T. Sri Vaishnavi, A. Melwin Raj, M. Narmatha, B. Naveena and P. Pratheesh Xavier

.

Abstract

COPD is a prevalent respiratory disease characterized by permanent airflow restriction and persistent inflammation in the small airways of the lungs in response to obnoxious environmental stimuli, typically cigarette smoke. Worldwide, COPD is ranked as the third most common cause of death and illness burden. COPD entails a spectrum of disorders, including chronic bronchitis and emphysema, with the majority of patients exhibiting symptoms of both. Bronchial infection caused by phagocytes, composed of neutrophils and macrophages, produces oxidants internally. In COPD, the diffused molecular law of HO-1 and its main protein regulators, which comprise of Nrf2, Bach1, and Keap1, is altered. In the United States, 12 million people are currently diagnosed with COPD. However, it is anticipated that at least an equal number of persons with altered lung features suggestive of COPD remain undetected. Inhaled irritants activate epithelial cells and alveolar macrophages, which release cytokines and chemokines and play a crucial role in airway inflammation. MMPs and neutrophil elastase, which are generated by alveolar macrophages and neutrophils, are responsible for elastin breakdown in the alveoli, which results in alveolar deterioration. No single mechanism can account for the complexity of COPD's pathophysiology. There are likely interactions between several processes.

Keywords: Chronic obstructive pulmonary disease, Oxidative stress, protease–anti- protease imbalance, Matrix metalloproteases, Inflammatory cells.