IP₃ R attenuates oxidative stress and inflammation damage in smoking-induced COPD by promoting autophagy.

ABSTRACT: Tobacco smoking is one of the most important risk factors for chronic obstructive pulmonary disease (COPD). However, the most critical genes and proteins remain poorly understood. Therefore, we aimed to investigate these hub genes and proteins in tobacco smoke-induced COPD, together with the potential mechanism(s). Differentially expressed genes (DEGs) were analysed between smokers and patients with COPD. mRNA expression and protein expression of IP₃ R were confirmed in patients with COPD and extracted smoke solution (ESS)-treated human bronchial epithelial (HBE) cells. Moreover, expression of oxidative stress, inflammatory cytokines and/or autophagy-related protein was tested when IP₃ R was silenced or overexpressed in ESS-treated and/or 3-MA-treated cells. A total o

SUBMITTER: Zhang Q 

PROVIDER: S-EPMC8256356 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature