ReviewMolecular biology reports2025
Pulmonary fibrosis and exosomes: pathways to treatment.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Advances in pharmacotherapy for fibrotic interstitial lung disease.Medical review (2021) · 2026Review
- Exosomes as Disease-Informed Nanoplatforms for Pulmonary Fibrosis: From Pathogenic Signaling to Precision Diagnosis and Therapy.Pharmaceutics · 2026Review
- Vitamin D receptor suppresses pulmonary fibroblast activation by downregulating the TGF-β1/Smad signaling pathway.Histochemistry and cell biology · 2026Article
- Unpacking the anti-fibrotic arsenal: molecular mechanisms and therapeutic translation of MSC-derived exosomes in pulmonary fibrosis.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive, life-threatening lung disease characterized by excessive extracellular matrix (ECM) deposition, fibroblast proliferation, and epithelial injury. Disease progression involves key signaling pathways-TGF-β, WNT/β-catenin, PI3K/AKT, and YAP/TAZ-that drive fibroblast activation, epithelial-to-mesenchymal transition (EMT), endothelial-mesenchymal transition (EndMT), and ECM remodeling. Recent studies have highlighted the role of small extracellular vesicles (sEVs), particularly exosomes, as crucial modulators of the fibrotic microenvironment. These vesicles carry microRNAs (miRNAs), proteins, and lipids that influence fibroblast behaviour, immune signaling, and tissue architecture.Growing evidence supports the therapeutic promise of exosomes and engineered nanoparticle-exosome hybrids in targeting dysregulated fibrotic pathways and promoting tissue repair. This review examines the molecular mechanisms underlying pulmonary fibrosis, focusing on the role of exosomal crosstalk and therapeutic potential. We also incorporate emerging insights from single-cell RNA sequencing (scRNA-seq) on fibroblast heterogeneity, the influence of senescence-associated secretory phenotype (SASP) on exosomal cargo, and the limitations of current animal models in recapitulating chronic IPF. Understanding these mechanisms may facilitate the development of precision medicine approaches for managing and potentially reversing IPF progression.
Indexed as
Identifiers
40699390What 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.