ArticleDrug design, development and therapy2022
Wnt/β-Catenin Participates in the Repair of Acute Respiratory Distress Syndrome-Associated Early Pulmonary Fibrosis via Mesenchymal Stem Cell Microvesicles.
Article in Drug design, development and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.
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
10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.
- Extracellular vesicles from mesenchymal stromal cells as a promising therapy for ARDS: a systematic review of preclinical studies.Frontiers in medicine · 2025Pooled it
- Safety, efficacy and biomarkers analysis of mesenchymal stromal cells therapy in ARDS: a systematic review and meta-analysis based on phase I and II RCTs.Stem cell research & therapy · 2022Pooled it
- MSCs/EVs-based therapy targeting DAD: research progress and future perspectives from ARDS and COVID-19 to RP-ILD.Stem cell research & therapy · 2026Review
- Gymnemagenin-3-O-glucuronide mitigates lipopolysaccharide-induced acute lung inflammation/injury by regulating the NF-κB/MAPK signalling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Mesenchymal stem cells and derived extracellular vesicles in major respiratory diseases: from multifaceted molecular mechanisms to clinical perspectives.Frontiers in cell and developmental biology · 2026Review
- Epithelial-mesenchymal transition in pulmonary fibrosis: molecular mechanisms and emerging therapeutic strategies.Frontiers in medicine · 2025Review
- Microvesicles derived from mesenchymal stem cells inhibit acute respiratory distress syndrome-related pulmonary fibrosis in mouse partly through hepatocyte growth factor.World journal of stem cells · 2024Article
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- Extracellular Vesicles in Idiopathic Pulmonary Fibrosis: Pathogenesis, Biomarkers and Innovative Therapeutic Strategies.International journal of nanomedicine · 2024Review
- Current status and prospects of basic research and clinical application of mesenchymal stem cells in acute respiratory distress syndrome.World journal of stem cells · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe main aim of the present study was to establish whether mesenchymal stem cell microvesicles (MSC MVs) exert anti-fibrotic effects and investigate the mechanisms underlying these effects in a mouse model of acute respiratory distress syndrome (ARDS)-associated early pulmonary fibrosis.
methodsAn ARDS-associated pulmonary fibrosis model was established in mice by an intratracheal injection of lipopolysaccharide (LPS). At 1, 3, and 7 days after LPS-mediated injury, the lungs of mice treated with MSC MVs and untreated controls were carefully excised and fibrosis was assessed based on the extent of collagen deposition. In addition, the development of epithelial-mesenchymal transition (EMT) was evaluated based on loss of E-cadherin and zona occludens-1 (ZO-1) along with the acquisition of α-smooth muscle actin (α-SMA) and N-cadherin. Nuclear translocation and β-catenin expression analyses were also used to evaluate activation of the Wnt/β-catenin signaling pathway.
resultsBlue-stained collagen fibers were evident as early as 7 days after LPS injection. Treatment with MSC MVs suppressed pathological progression to a significant extent. MSC MVs markedly reversed the upregulation of N-cadherin and α-SMA and attenuated the downregulation of E-cadherin and ZO-1. The expression and nuclear translocation of β-catenin were clearly decreased on day 7 after MSC MV treatment.
conclusionAnalyses indicated that MSC MVs could ameliorate ARDS-associated early pulmonary fibrosis via the suppression of EMT and might be related to Wnt/β-catenin transition signaling.
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.