Participación de las metaloproteinasas de matriz extracelular en la EPOC

Abstract

In chronic obstructive pulmonary disease (COPD) are two clinical phenotypes, emphysema and chronic bronchitis. Phenotypes share clinical symptoms such as dyspnea and bronchial obstruction to air flow and an increase of innate immune cells (macrophages and neutrophils), the release of multiple inflammatory mediators (chemokines, cytokines, and growth factors), oxidative stress, increased extracellular matrix metalloproteinases (MMPs) in the airways and lung. Disease progression is associated with the presence of chronic inflammation and increased proteolytic activity of enzymes such as MMPs resulting in the degradation of elastin and collagen fibers in the walls of the alveoli and the lung’s extracellular matrix. Of particular interest for this review was to describe the role of MMPs, their participation in the development of COPD, both in the extracellular matrix destruction and abnormal lung remodeling damaged. Also mentioned genetic association studies of polymorphisms in MMPs type SNP in Caucasian populations such as the development and progression of COPD, and the importance of carrying out studies in Mexican mestizo population. The role of MMPs has also been known through animal models and knockout mice MMPs exposed to cigarette smoke. All these studies implicate MMPs as key mediators in the pathogenesis of COPD. Finally, the study of MMPs base allow for future therapies, potential therapeutic targets and disease treatments.