ArticleFrontiers in cell and developmental biology2021
Capillarized Liver Sinusoidal Endothelial Cells Undergo Partial Endothelial-Mesenchymal Transition to Actively Deposit Sinusoidal ECM in Liver Fibrosis.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026Review
- Deletion of the mouse myocardial Nppb gene alleviates sepsis-induced myocardial dysfunction.Journal of molecular histology · 2026Article
- Mechanobiological feedback loops and quantitative decision thresholds in organ fibrosis: Translational principles for antifibrotic therapy.Journal of cell communication and signaling · 2026Review
- Review
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
- Article
- Liver sinusoidal endothelial TGF-β signaling accelerates partial endothelial-mesenchymal transition and MASH through Notch.JHEP reports : innovation in hepatology · 2026Article
- Periodontitis and Chronic Liver Disease: Mechanistic Insights Focusing onMicroorganisms · 2026Review
- Endothelial Cell Therapy for the Acute and Chronic Liver Disease.Seminars in liver disease · 2026Review
- Automating Vascular Biology: An End-to-End Automated Workflow for High-Throughput Blood Vessel-on-a-Chip Production and Multi-Site Validation.Advanced healthcare materials · 2026Article
- Endothelial-to-Mesenchymal Transition in Health and Disease: Molecular Insights and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Interleukin 33 Promotes Liver Sinusoidal Endothelial Cell Dysfunction and Hepatic Fibrosis in Diabetic Mice.Diabetes & metabolism journal · 2025Article
- Deciphering the role ofWorld journal of hepatology · 2025Review
- miR-27b-3p modulates liver sinusoidal endothelium dedifferentiation in chronic liver disease.Hepatology communications · 2025Article
- Liver Sinusoidal Endothelial Cells in the Regulation of Immune Responses and Fibrosis in Metabolic Dysfunction-Associated Fatty Liver Disease.International journal of molecular sciences · 2025Review
- Non-parenchymal cells: key targets for modulating chronic liver diseases.Frontiers in immunology · 2025Review
- Integrating single-cell RNA sequencing with spatial transcriptomics reveal the fibrosis-related genes in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Angiocrine signaling in sinusoidal homeostasis and liver diseases.Journal of hepatology · 2024Review
- Transcriptome Analyses of Liver Sinusoidal Endothelial Cells Reveal a Consistent List of Candidate Genes Associated with Endothelial Dysfunction and the Fibrosis Progression.Current issues in molecular biology · 2024Article
- Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis.Clinical and molecular hepatology · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tissue-specific endothelial cells are more than simply a barrier lining capillaries and are proved to be capable of remarkable plasticity to become active collagen matrix-producing myofibroblasts (MFs) in solid organs with fibrosis. Liver sinusoidal endothelial cells (LSECs) also participate in the development of hepatic fibrosis, but the exact roles and underlying mechanism have been poorly understood in addition to capillarization. In this study, we demonstrate, by using single-cell RNA sequencing, lineage tracing, and colocalization analysis, that fibrotic LSECs undergo partial endothelial mesenchymal transition (EndMT) with a subset of LSECs acquiring an MF-like phenotype. These phenotypic changes make LSECs substantial producers of extracellular matrix (ECM) preferentially deposited in liver sinusoids but not septal/portal scars as demonstrated by immunofluorescence in animal models and patients with fibrosis/cirrhosis, likely due to their limited migration. Bioinformatic analysis verifies that LSECs undergo successive phenotypic transitions from capillarization to mesenchymal-like cells in liver fibrosis. Furthermore, blockade of LSEC capillarization by using YC-1, a selective eNOS-sGC activator, effectively attenuates liver damage and fibrogenesis as well as mesenchymal features of LSECs, suggesting that capillarization of LSECs might be upstream to their mesenchymal transition during fibrosis. In conclusion, we report that capillarized LSECs undergo a partial EndMT characterized by increased ECM production without activating cell mobility, leading to perisinusoidal ECM deposition that aggravate liver function and fibrogenesis. Targeting this transitional process may be of great value for antifibrotic treatment of liver fibrosis.
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