AI Article Synopsis
- Cigarette smoking is the primary cause of chronic obstructive pulmonary disease (COPD), but the exact biological processes that lead to lung function decline are still unclear.
- Researchers identified 1758 tryptic peptides in plasma samples from smokers using advanced mass spectrometry techniques, focusing on how these relate to changes in lung function.
- analysis revealed 30 peptides associated with the rate of lung function decline in smokers, indicating that certain proteins linked to immune response and metabolism may play a role in the progression of COPD related to smoking.
Article Abstract
Although cigarette smoking is recognized as the most important cause of chronic obstructive pulmonary disease (COPD), the pathophysiological mechanisms underlying the lung function decline are not well understood. Using off-line strong cation exchange fractionation with RP-LC-ESI-MS/MS and robust database searching, 1758 tryptic peptides were identified in plasma samples from cigarette smokers. Using two statistical approaches, 30 peptides were identified to be associated with the annualized rate of lung function decline over 5 years among smokers with COPD characterized as having rapid (n = 18) or slow (n = 18) decline and 18 smokers without COPD. The identified peptides belong to proteins that are involved in the complement or coagulation systems or have antiprotease or metabolic functions. This research demonstrates the utility of proteomic profiling to improve the understanding of molecular mechanisms involved in cigarette smoking-related COPD by identifying plasma proteins that correlate with decline in lung function.
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| http://dx.doi.org/10.3109/13547501003789901 | DOI Listing |
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