ArticleTransplantation direct2025
Proteomic Analysis of Transbronchial Biopsies to Discover Novel Biomarkers for Early Identification of Chronic Lung Allograft Dysfunction.
Article in Transplantation direct, 2025. 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.
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Who cites it
2 citing papers in PubMed.
- Lung transplantation in 2025: a narrative review of progress, challenges, and the road ahead.Journal of thoracic disease · 2026Review
- Role of MZB1 in disease pathogenesis: current insights and future directions.Clinical and experimental medicine · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chronic lung allograft dysfunction (CLAD) is a major contributor to poor long-term survival after lung transplantation (LTx). There is a paucity of validated tissue biomarkers which limits the early detection of CLAD. The aim of this study was to discover novel tissue proteins in CLAD. Methods: A longitudinal cohort study analyzed 15 tissue specimens from 2 groups of bilateral LTx recipients; those with CLAD (n = 3) and those without CLAD (n = 3). In both groups, transbronchial biopsies (TBBx) were retrieved from 2 timepoints; stable surveillance at 90 d after transplant, and during episodes of acute lung allograft dysfunction. In the CLAD cohort, additional tissue from explant CLAD lungs collected at retransplantation was analyzed. Proteomics analysis and immunohistochemistry were used to identify and validate differentially expressed proteins. Results: Tissue upregulation of a number of proteins including SerpinB1, SerpinH1, Cofilin 1, MUC1, COL15A1, COL4A4, and Coronin1B was found in recipients with CLAD. This finding was present when comparing CLAD onset and explant pathology to stable surveillance among recipients with CLAD and evident when compared with recipients without CLAD. Most of the upregulated tissue proteins in patients with CLAD had collectively critical roles in leukocytes migration and activation, inflammation, free radicals production and oxidative stress, epithelial-mesenchymal transition, myofibroblasts activation, and excessive deposition of extracellular matrix, which in turn enhance the risk of lung fibrosis and graft rejection. We also found exclusive expression of HLA-DQB1, JCHAIN, SAP18, FUCA1, MZB1, G3BP2, and BTF3 in CLAD cases, indicating they could be specific biomarkers of CLAD. Conclusions: This study identifies distinct proteomes that are linked to CLAD development and consequently may be a useful indicator for identifying LTx patients at higher risk of CLAD.
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Registered trials
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