Experimental therapeutics of Nrf2 as a target for prevention of bacterial exacerbations in COPD.

ABSTRACT: A growing body of evidence indicates that oxidative stress plays a central role in the progression of chronic obstructive pulmonary disease (COPD). Chronic oxidative stress caused by cigarette smoke generates damage-associated molecular patterns (DAMPs), such as oxidatively or nitrosatively modified proteins and extracellular matrix fragments, which induce abnormal airway inflammation by activating innate and adaptive immune responses. Furthermore, oxidative stress-induced histone deacetylase 2 (HDAC2) inactivity is implicated in amplifying inflammatory responses and corticosteroid resistance in COPD. Oxidative stress also mediates disruption of innate immune defenses, which is associated with acute exacerbation of COPD. Host defense transcription factor Nuclear factor erythroid 2-related

SUBMITTER: Biswal S 

PROVIDER: S-EPMC3359107 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature