ArticleJournal of cellular and molecular medicine2020
Low let-7d exosomes from pulmonary vascular endothelial cells drive lung pericyte fibrosis through the TGFβRI/FoxM1/Smad/β-catenin pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Systematic review of extracellular vesicle-derived microRNAs involved in organ fibrosis: implications for arthrofibrosis therapy.Journal of translational medicine · 2025Pooled it
- How extracellular vesicles contribute to pulmonary fibrosis: miRNA-mediated mechanisms, diagnostic potential, and emerging therapeutic strategies.Molecular biology reports · 2026Review
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Exosomes as Disease-Informed Nanoplatforms for Pulmonary Fibrosis: From Pathogenic Signaling to Precision Diagnosis and Therapy.Pharmaceutics · 2026Review
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- Integrative Metabolomic, Network Pharmacology, and Experimental Evidence forPharmaceuticals (Basel, Switzerland) · 2025Article
- Circulating MicroRNAs in Idiopathic Pulmonary Fibrosis: A Narrative Review.Current issues in molecular biology · 2024Review
- Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Alveolar Organoids in Lung Disease Modeling.Biomolecules · 2024Review
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Extracellular Vesicles in Idiopathic Pulmonary Fibrosis: Pathogenesis, Biomarkers and Innovative Therapeutic Strategies.International journal of nanomedicine · 2024Review
- Role of transcription factor FOXM1 in diabetes and its complications (Review).International journal of molecular medicine · 2023Article
- Extracellular vesicles: emerging roles, biomarkers and therapeutic strategies in fibrotic diseases.Journal of nanobiotechnology · 2023Review
- Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Protective role of FBXL19 in Streptococcus pneumoniae-induced lung injury in pneumonia immature mice.Journal of cardiothoracic surgery · 2023Article
- LncRNA GAS5 suppresses TGF-β1-induced transformation of pulmonary pericytes into myofibroblasts by recruiting KDM5B and promoting H3K4me2/3 demethylation of the PDGFRα/β promoter.Molecular medicine (Cambridge, Mass.) · 2023Article
- (-)‑Epigallocatechin‑3‑Biomedical reports · 2023Article
- Therapeutic use of calpeptin in COVID-19 infection.Clinical science (London, England : 1979) · 2022Article
- Recent Advances in Molecular Diagnosis of Pulmonary Fibrosis for Precision Medicine.ACS pharmacology & translational science · 2022Review
- The oncogenic landscape of the idiopathic pulmonary fibrosis: a narrative review.Translational lung cancer research · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of pulmonary fibrosis (PF) was mediated by the progressive deposition of excessive extracellular matrix, but little is known about the regulatory mechanisms of fibrogenesis by lung pericytes. The mouse PF model was established by treatment with bleomycin, followed by isolation of exosomes from mouse broncho-alveolar lavage fluids by the centrifuge method. Relative mRNA/microRNA levels and protein expression were assessed by qRT-PCR and Western blotting, respectively. The binding of let-7d with gene promoter was validated by dual-luciferase reporter assay. Protein interactions were verified via GST pull-down and co-immunoprecipitation. Nuclear retention of Smad3 was analysed by extraction of cytoplasmic and nuclear fraction of pericytes followed by Western blotting. Association of FoxM1 with gene promoter was detected by EMSA and ChIP-PCR methods. FoxM1 expression is significantly elevated in human lung fibroblasts of PF patients and mouse PF model. The expression of let-7d is repressed in exosomes derived from broncho-alveolar lavage fluids of PF mice. Let-7d or FoxM1 knockdown suppressed the expression of FoxM1, Smad3, β-catenin, Col1A and α-SMA expression in mouse lung pericytes under TGF-β1 treatment. FoxM1 overexpression elevated above gene expression in mouse lung pericytes under TGF-β1 treatment. Let-7d directly targets TGFβRI to regulate FoxM1 and downstream gene expression in mouse lung pericytes. FoxM1 directly interacts with Smad3 proteins to promote Smad3 nuclear retention and binds with β-catenin promoter sequence to promote fibrogenesis. Exosomes with low let-7d from pulmonary vascular endothelial cells drive lung pericyte fibrosis through activating the TGFβRI/FoxM1/Smad/β-catenin signalling pathway.
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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 OpenQuestion graph.