ArticleCell death & disease2019
Hepatocyte-derived exosomal MiR-194 activates PMVECs and promotes angiogenesis in hepatopulmonary syndrome.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 52 citations in OpenAlex.
- Look Who Is Talking: Extracellular Vesicles as Mediators of Intercellular and Interorgan Communication.Comprehensive Physiology · 2026Review
- SerpinB1a induces hepatopulmonary syndrome by promoting CTSG/AMPK/mTOR pathway-mediated mitophagy.Cell biology and toxicology · 2025Article
- Crosstalk between lung and extrapulmonary organs in sepsis-related acute lung injury/acute respiratory distress syndrome.Annals of intensive care · 2025Review
- Disruption of Hepatic Sinusoidal Homeostasis Leads to Hepatopulmonary Syndrome.Journal of cellular and molecular medicine · 2025Review
- Extracellular vesicle-mediated bidirectional communication between the liver and other organs: mechanistic exploration and prospects for clinical applications.Journal of nanobiotechnology · 2025Review
- MiR-25-3p regulates pulmonary arteriovenous malformation after Glenn procedure in patients with univentricular heart via the PHLPP2-HIF-1α axis.Scientific reports · 2025Article
- Article
- Emerging Evidence Linking the Liver to the Cardiovascular System: Liver-derived Secretory Factors.Journal of clinical and translational hepatology · 2023Review
- Serum Soluble Vascular Endothelial Growth Factor Receptor 1 as a Potential Biomarker of Hepatopulmonary Syndrome.Journal of clinical and translational hepatology · 2023Article
- Vascular Extracellular Vesicles Indicate Severe Hepatopulmonary Syndrome in Cirrhosis.Diagnostics (Basel, Switzerland) · 2023Article
- Systemic Metabolic Alteration Dependent on the Thyroid-Liver Axis in Early PD.Annals of neurology · 2023Article
- The right ventricle in tetralogy of Fallot: adaptation to sequential loading.Frontiers in pediatrics · 2023Review
- Fractalkine modulates pulmonary angiogenesis and tube formation by modulating CX3CR1 and growth factors in PVECs.Open life sciences · 2023Article
- Circulating Extracellular Vesicles Contain Liver-Derived RNA Species as Indicators of Severe Cholestasis-Induced Early Liver Fibrosis in Mice.Antioxidants & redox signaling · 2022Article
- Tumor microenvironment pathways: Cross regulation in breast cancer metastasis.Genes & diseases · 2022Review
- Endothelial glycocalyx in hepatopulmonary syndrome: An indispensable player mediating vascular changes.Frontiers in immunology · 2022Review
- Role of extracellular vesicles in liver diseases and their therapeutic potential.Advanced drug delivery reviews · 2021Review
- Linc-ROR promotes the progression of breast cancer and decreases the sensitivity to rapamycin through miR-194-3p targeting MECP2.Molecular oncology · 2020Article
- [Diagnosis and therapeutic strategies for hepatopulmonary syndrome].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020Article
- Dying tumor cell-derived exosomal miR-194-5p potentiates survival and repopulation of tumor repopulating cells upon radiotherapy in pancreatic cancer.Molecular cancer · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatopulmonary syndrome (HPS) is a serious vascular complication in the setting of liver disease. Factors produced by the liver are essential to regulate pulmonary angiogenesis in the pathogenesis of HPS; however, the pathogenic mechanisms of pulmonary angiogenesis are not fully understood. We investigated the role of HPS rat serum exosomes (HEs) and sham-operated rat serum exosomes (SEs) in the regulation of angiogenesis. We found that HEs significantly enhance PMVEC proliferation, migration, and tube formation. We further identified miR-194 was the most notably increased miRNA in HEs compared to SEs. Once released, hepatocyte-derived exosomal miR-194 was internalized by PMVECs, leading to the promotion of PMVEC proliferation, migration, and tube formation through direct targeting of THBS1, STAT1, and LIF. Importantly, the pathogenic role of exosomal miR-194 in initiating angiogenesis was reversed by P53 inhibition, exosome secretion inhibition or miR-194 inhibition. Additionally, high levels of miR-194 were found in serum exosomes and were positively correlated with P(A-a)O
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