ArticleJournal of extracellular vesicles2026
Myofibroblast-Derived Extracellular Vesicles Drive Profibrotic Cascade Amplification in Pulmonary Fibrosis via the Nestin-Rab7 Axis.
Article in Journal of extracellular vesicles, 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.
- How extracellular vesicles contribute to pulmonary fibrosis: miRNA-mediated mechanisms, diagnostic potential, and emerging therapeutic strategies.Molecular biology reports · 2026Review
- Engineered NestinJournal of extracellular vesicles · 2026Article
- Myofibroblast-Derived Extracellular Vesicles Drive Profibrotic Cascade Amplification in Pulmonary Fibrosis via the Nestin-Rab7 Axis.Journal of extracellular vesicles · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a fatal fibrotic lung disease characterized by aberrant myofibroblast activation and excessive extracellular matrix deposition, with extracellular vesicles (EVs) playing a crucial role in this pathological process. We observed that EVs levels are significantly elevated in IPF and positively correlate with nestin expression, a known marker of lung myofibroblasts. These myofibroblast-derived EVs further amplify profibrotic responses, creating a self-perpetuating cycle. To elucidate the mechanisms driving increased EVs secretion, we conducted in vitro and in vivo experiments, demonstrating that nestin knockdown not only suppresses EVs release but also impairs their ability to promote TGF-β-induced myofibroblast differentiation. Mechanistically, nestin recruits TBC1D15 to inactivate Rab7, thereby inhibiting multivesicular body (MVB) degradation and enhancing EVs secretion. Importantly, pharmacological activation of Rab7 using ML-098 significantly attenuated pulmonary fibrosis in mouse models. Our findings establish the Nestin-Rab7 axis as a key regulator of EVs-mediated fibrotic signaling and highlight its therapeutic potential for IPF treatment.
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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.