ReviewLung2026
The Pleural Microenvironment in Pulmonary Injury and Fibrosis: Mechanistic Insights and Links to Tissue Repair.
Review in Lung, 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
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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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe pleural microenvironment has long been considered a passive anatomical boundary. However, emerging evidence identifies it as an active regulator of inflammation, tissue repair, and fibrotic remodeling. This review evaluates the mechanistic contribution of pleural mesothelial cells (PMCs) to pulmonary injury and fibrosis and explores their potential role in coordinating regenerative responses.
methodsRecent preclinical and clinical studies investigating pleural biology, mesothelial plasticity, mesothelial-mesenchymal transition (MesoMT), and pulmonary fibrosis were critically analyzed. Evidence from cutaneous wound healing was integrated to identify common molecular pathways governing tissue repair and fibrotic progression
resultsPMCs actively participate in pulmonary remodeling by secreting cytokines, growth factors, and extracellular matrix regulators. Persistent activation of TGF-β/Smad, Wnt/β-catenin, PI3K/Akt, and IL-6/STAT3 signaling promotes MesoMT, myofibroblast accumulation, and progressive extracellular matrix deposition in pulmonary fibrosis. Conversely, pleural-derived mediators have demonstrated regenerative potential by enhancing epithelial proliferation, migration, angiogenesis, and tissue repair in experimental models. Collectively, current evidence suggests that pleural signaling functions as a context-dependent regulatory network that influences the transition between effective regeneration and pathological fibrosis
conclusionThe pleura can be regarded as a dynamic signaling niche that extends beyond its traditional structural role. We propose the pleural microenvironment as a regulatory interface governing the balance between tissue regeneration and fibrotic remodeling. Targeting pleural-derived signaling networks may provide novel therapeutic opportunities for restoring physiological repair while limiting fibrotic progression in chronic lung diseases.
Indexed as
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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.