Role of Oxidative Stress and Genetic Polymorphism of Matrix Metalloproteinase-2 and Tissue Inhibitor of Metalloproteinase-2 in COPD.

ABSTRACT

Chronic obstructive pulmonary disease (COPD), a complaint described by progressive and inadequately reversible limitation in lungs with systemic inflammation, is largely current in India. There's no remedy available so far it is, thus, imperative to understand the underpinning pathogenesis of the complainant. A set of proteases known as Matrix metalloproteinase (MMPs) are especially involved in the process of alveolar destruction and mucus hypersecretion. There are responsible factors in an inheritable position to control COPD like MMPs and TIMPs (Tissue Inhibitor of Metalloproteinases). MMPs degrade extracellular matrix and lead to the pathogenesis of COPD [1]. TIMPs proteins that help to inhibit the Matrix metalloproteinases. [2]. This review summarizes the implicit part of crucial MMP-2 and TIMP-2 in COPD disease. Though the concept seems promising, limited knowledge about the exact functions of a particular MMP in COPD and the complications of MMP in substrate affinity makes this a grueling task. MMP2 and TIMP2 both are directly or indirectly regulated by oxidative stress and epigenetic mechanism which regulates their expressions. COPD is a seditious response to factors like dust, smoke, etc., and triggers extra-pulmonary goods which cause inflammation. [3]. This review explains the relationship between MMP2 and TIMP2 in COPD patients with oxidative stress, its impact on COPD pathogenesis, and gene expression of TIMP2 and MMP2 with their downstream effects. This also gives some insights into therapeutic interventions for targeting these enzymes. MMP2 and TIMP2 both play a role in the development of COPD and they need to be studied with the utmost focus.