ArticleGeroScience2026
Plasma proteomic biomarkers as mediators for the associations between frailty phenotypes and chronic respiratory diseases.
Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Association between frailty and the risks of chronic pulmonary diseases and lung cancer.BMC pulmonary medicine · 2026Article
- Proteomic signals are not equal clinical phenotypes: redefining evidence standards in arbovirus-SARS-CoV-2 cross-reactivity.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Frailty, a hallmark of systemic vulnerability in aging populations, is increasingly recognized in the clinical management of chronic respiratory diseases (CRDs). Molecular mechanism underpinning the relationships remain insufficiently elucidated. This study hence aimed to investigate whether proteomic biomarkers-circulating plasma proteins reflecting systemic inflammation, metabolism, and tissue remodeling-are associated with CRDs and may serve as potential mediators of the observed links. We analyzed data from a population-based cohort of 22,802 adults with proteomic measurements. Frailty was assessed by three phenotypes, including frailty index, physical frailty, and psychological frailty. Related-proteomic signatures were estimated by both linear and elastic regression models. Cox regression models were applied to explore the associations of frailty phenotypes and their proteomic signatures with incident CRDs, including asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF), as well as lung function outcomes, with full adjustments for potential confounders. Furthermore, mediation analyses were conducted to explore underlying mechanisms, complemented by pathway enrichment analyses to reveal relevant biological functions. Over a median follow-up of 13.2 years, 617 participants developed asthma, 701 developed COPD, and 228 developed IPF. Higher frailty index was associated with elevated risks of asthma (HR 1.95, 95% CI 1.64 to 2.31) and COPD (2.02, 1.71 to 2.38). Corresponding proteomic signature also related to increased risks of asthma (HR 1.22, 1.11 to 1.34) and COPD (1.65, 1.53 to 1.78). Mediation analysis suggested that the frailty index partially mediated the association with COPD, accounting for 26.0% (95% CI: 18.7 to 37.5%) of the total effect, respectively, particularly for GDF15, WFDC2, and PLAUR. Pathway enrichment analysis showed that these mediating proteins were predominantly involved in immune activation, inflammatory signaling, and metabolic stress responses. Frailty phenotypes contribute to elevated CRDs risks, partly through proteomic dysregulation in inflammatory and metabolic pathways.
Indexed as
Identifiers
41639365What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.