ArticleOrphanet journal of rare diseases2026
CCL14, identified by multi-omics approach, serves as a novel indicator of disease severity and progression in lymphangioleiomyomatosis.
Article in Orphanet journal of rare diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLymphangioleiomyomatosis (LAM) is a rare, multisystemic metastatic disease. Chemokines are implicated in promoting LAM cell migration and tumor progression. Our prior plasma proteomics identified elevated C-C motif chemokine ligand 14 (CCL14) in LAM, yet its role remains unexplored.
methodsProteomic analysis identified CCL14 as differentially expressed in LAM patients versus healthy controls. Single-cell RNA sequencing (scRNA-seq) of lung tissues (six LAM patients, five healthy donors) identified the cellular source of CCL14 and explored its functional pathways bioinformatically. ELISA-quantified plasma CCL14 levels were analyzed for correlations with clinical phenotypes and longitudinal disease progression in 53 LAM patients and 25 controls.
resultsProteomics and scRNA-seq revealed upregulation of CCL14 in LAM patients, primarily localized to lymphatic and vascular endothelial cells. Functional enrichment linked CCL14 to proliferative (mTORC1, MYC), inflammatory (TNF-α/NF-κB), and chemotactic pathways. CellPhoneDB indicated CCL14 mediates interactions between endothelial cells and innate immune/alveolar epithelial cells, and between endothelial cells themselves, via ACKR2, CCR3 and CCR1. Clinically, plasma CCL14 levels were significantly elevated in LAM patients versus controls (p = 0.003). Subgroup analyses demonstrated higher CCL14 levels in patients with angiomyolipomas (AMLs) versus those without, and in CT grade III versus grade I/II. Critically, CCL14 predicted disease progression: baseline CCL14 levels were higher in progressive versus stable patients (p = 0.0266) and positively correlated with annual increase in the percentage of cystic lung volume (r = 0.4051, p = 0.0446).
conclusionsCCL14 is a critical regulatory molecule within the LAM microenvironment and a promising biomarker for disease severity and progression.
Indexed as
Identifiers
What 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.