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- W2344474925 endingPage "45" @default.
- W2344474925 startingPage "S138" @default.
- W2344474925 abstract "Accumulation of nonfunctional and potentially cytotoxic, misfolded proteins in chronic obstructive pulmonary disease (COPD) is believed to contribute to lung cell apoptosis, inflammation, and autophagy. Because of its fundamental role as a quality control system in protein metabolism, the unfolded protein response (UPR) is of potential importance in the pathogenesis of COPD. The UPR comprises a series of transcriptional, translational, and post-translational processes that decrease protein synthesis while enhancing protein folding capacity and protein degradation. Several studies have suggested that the UPR contributes to lung cell apoptosis and lung inflammation in at least some subjects with human COPD. However, information on the prevalence of the UPR in subjects with COPD, the lung cells that manifest a UPR, and the role of the UPR in the pathogenesis of COPD is extremely limited and requires additional study." @default.
- W2344474925 created "2016-06-24" @default.
- W2344474925 creator A5074783469 @default.
- W2344474925 date "2016-04-01" @default.
- W2344474925 modified "2023-09-29" @default.
- W2344474925 title "The Unfolded Protein Response in Chronic Obstructive Pulmonary Disease." @default.
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- W2344474925 doi "https://doi.org/10.1513/annalsats.201506-320kv" @default.
- W2344474925 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5015720" @default.
- W2344474925 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27115948" @default.
- W2344474925 hasPublicationYear "2016" @default.
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