ArticleRespiratory research2026
Single-cell RNA sequencing elucidates potential mechanisms of endothelial cells in lung region-specific repair and remodeling in combined pulmonary fibrosis and emphysema.
Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Endothelial Atypical Receptors for Chemoattractants in Lung Immune Surveillance.European journal of immunology · 2026Review
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 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
12 authors.
Funding
Abstract
backgroundCombined pulmonary fibrosis and emphysema (CPFE) is a severe and progressive lung disease with limited therapeutic options and poor prognosis. CPFE manifests as emphysema and fibrosis in different lung regions and is frequently associated with pulmonary hypertension. Pulmonary vascular endothelial cells may regulate these processes, but their role in CPFE remains unclear.
methodsSingle-cell RNA sequencing and multiplex immunohistochemistry were performed on upper/lower lung tissues from CPFE patients and healthy controls. Cellular heterogeneity, gene expression, and intercellular communication networks were analyzed.
resultsThe upper lung of CPFE exhibited marked depletion and impaired function of endothelial cells, along with neutrophil accumulation and M1 macrophage-driven inflammation. Conversely, the lower lung of CPFE displayed higher proportions of ACKR1 + venous endothelial cells and enhanced angiogenesis. Endothelial cells demonstrated profibrotic signaling via THBS1-SDC4, PDGFB-PDGFRα, and JAG1-NOTCH3 signaling targeting epithelial cells, fibroblasts, and smooth muscle cells, respectively. These endothelial cells also exhibited strong interactions with macrophages through chemokines and adhesion molecules such as CCL14 and ICAM1, and expressed factors promoting M2 macrophage polarization. Multi-color staining confirmed the proximity of these endothelial cells with specific lung resident cells and immune cells, with clear spatial compartmentalization of endothelial cells with their target cell populations in the upper and lower lungs of CPFE.
conclusionsThis study provides a preliminary cellular characterization of CPFE, implicating endothelial cells as potential regulators of its regional pathology through angiocrine signaling and macrophage crosstalk. The findings provide novel mechanistic insights into the histopathological heterogeneity of CPFE and highlight these pathways as therapeutic targets.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.