ArticleMedicine2026
Causal effects of circulating inflammatory proteins on COPD: A Mendelian randomization study.
Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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7 authors.
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Abstract
Chronic obstructive pulmonary disease (COPD) is a major public health concern due to its high prevalence, morbidity, and mortality. Although COPD is recognized as a systemic inflammatory disease, the specific circulating inflammatory proteins associated with its development and progression remain poorly understood. We performed a Mendelian randomization (MR) study to investigate the association between circulating inflammatory proteins and COPD risk. Genetic data were obtained from a genome-wide association study of 20,066 COPD cases and 338,303 controls from the FinnGen consortium and circulating inflammatory protein data were derived from a genome-wide association study of 14,824 participants. The inverse-variance weighted method was used as the primary analysis. Depending on the number of available instrumental variables, complementary methods including the Wald ratio, Weighted Median, MR-Egger, Weighted Mode, and Simple Mode were applied to assess robustness. Sensitivity analyses were conducted to evaluate heterogeneity and pleiotropy using Cochran's Q test, the MR-Egger intercept, MR-PRESSO, and leave-one-out analysis. In addition, cis-acting protein quantitative trait locus -restricted analyses were performed to further reduce potential pleiotropy. Our findings showed that higher genetically predicted levels of CCL28 (odds ratio [OR] = 0.83, 95% confidence interval [CI]: 0.69-0.99, P = .0394), CD40 (OR = 0.94, 95% CI: 0.89-0.99, P = .0170), and urokinase-type plasminogen activator (OR = 0.91, 95% CI: 0.85-0.99, P = .0212) were associated with a lower risk of COPD, whereas higher levels of Flt3L (OR = 1.09, 95% CI: 1.01-1.18, P = .0344) and CD6 (OR = 1.06, 95% CI: 1.02-1.12, P = .0099) were associated with a higher risk. Sensitivity analyses showed no evidence of heterogeneity or directional pleiotropy, and leave-one-out analyses indicated that the results were not driven by any single nucleotide polymorphism. These findings suggest that circulating inflammatory proteins, including CCL28, CD40, urokinase-type plasminogen activator, Flt3L, and CD6, may be involved in COPD pathogenesis. Further studies are needed to validate these findings and clarify their potential biological relevance.
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