Objective: COPD is the most common chronic respiratory disease with complex environmental and genetic etiologies. It was reported that might participate in the occurrence and development of respiratory diseases. However, the association between and COPD was unclear.
Methods: First, a case-control study enrolling 1130 COPD patients and 1115 healthy controls in Guangzhou was conducted to clarify the association between polymorphisms and COPD susceptibility. Secondly, a prevalence study recruited 882 participants in Gansu to verify the effect of positive polymorphisms on lung function. Finally, the 10-year absolute risk considering environmental factors and genetic variations was calculated by the method of Gail and Bruzzi.
Results: rs13419896 AA genotype reduced COPD risk in southern Chinese (AA vs. GG: adjusted OR = 0.689, 95% CI = 0.498-0.955; AA vs. GG/GA: adjusted OR = 0.701, 95% CI = 0.511-0.962). Further, the rs13419896 A allele was significantly associated with higher pre-FEV1/pre-FVC in both the Guangzhou and Gansu populations ( < 0.05). Smoking status, coal as fuels, education level, and rs13419896 G > A were finally retained to develop a relative risk model for males. Smoking status, biomass as fuels, and rs13419896 G > A were retained in the female model. The population-attributable risk of the male or female model was 0.457 (0.283-0.632) and 0.421 (0.227-0.616), respectively.
Conclusions: This study first revealed that rs13419896 G > A decreased COPD susceptibility and could be a genetic marker to predict the 10-year absolute risk for COPD.
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http://dx.doi.org/10.1016/j.heliyon.2023.e20226 | DOI Listing |
Int J Chron Obstruct Pulmon Dis
January 2025
Department of Rehabilitation Medicine, General Hospital of Central Theater Command, Wuhan, 430065, People's Republic of China.
Background: In preliminary research and literature review, we identified a potential link between chronic obstructive pulmonary disease (COPD) and lipid metabolism. Therefore, this study employed Mendelian randomization (MR) analysis to investigate the potential causal connection between blood lipids and COPD.
Materials And Methods: A genome-wide association study (GWAS) on COPD was conducted, encompassing a total of 112,583 European participants from the MRC-IEU.
Int J Rheum Dis
January 2025
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Army Medical University, Chongqing, China.
Background: Airway inflammation is considered one of the pathogenic factors in rheumatoid arthritis (RA), but the role of chronic obstructive pulmonary disease (COPD) in the development of RA remains unclear. We used cross-sectional studies and Mendelian randomization (MR) analysis to explore the link between COPD and RA.
Methods: In National Health and Nutrition Examination Survey (NHANES) 2013-2018, the association between COPD and RA was investigated using weighted logistic regression models.
Biol Direct
January 2025
Key Laboratory of Geriatrics of Jiangsu Province, Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu, China.
Background: Despite the increasing body of evidence that mitochondrial activities implicate in chronic obstructive pulmonary disease (COPD), we are still far from a causal-logical and mechanistic understanding of the mitochondrial malfunctions in COPD pathogenesis.
Results: Differential expression genes (DEGs) from six publicly available bulk human lung tissue transcriptomic datasets of COPD patients were intersected with the known mitochondria-related genes from MitoCarta3.0 to obtain mitochondria-related DEGs associated with COPD (MitoDEGs).
Respir Res
January 2025
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, 150081, People's Republic of China.
Background: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease, influenced by both environmental and genetic factors. Single nucleotide polymorphism (SNP) in the human genome may influence the risk of developing COPD and the response to treatment. We assessed the effects of gene polymorphism of inflammatory and immune-active factors and gene-environment interaction on risk of COPD in middle-aged and older Chinese individuals.
View Article and Find Full Text PDFDiagnostics (Basel)
December 2024
Computer Science Department, Taif University, Taif 21944, Saudi Arabia.
: In the United States, chronic obstructive pulmonary disease (COPD) is a significant cause of mortality. As far as we know, it is a chronic, inflammatory lung condition that cuts off airflow to the lungs. Many symptoms have been reported for such a disease: breathing problems, coughing, wheezing, and mucus production.
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