ArticleMolecular medicine (Cambridge, Mass.)2020
Exosomal miR-223 derived from natural killer cells inhibits hepatic stellate cell activation by suppressing autophagy.
Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 63 citations in OpenAlex.
- Review
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- NK-cell-derived exosomes exert antitumor potency via miR-140/XYLT1/HSPG2 axis.Cellular & molecular biology letters · 2026Article
- Encapsulation of hydroxyurea in exosomes derived from adipose mesenchymal stem cells enhances anticancer efficacy in breast cancer.Translational oncology · 2026Article
- Extracellular Vesicles in Liver Disease: Redefining Diagnostic and Therapeutic Strategies.International journal of stem cells · 2026Review
- Extracellular Vesicles in Liver Fibrosis: Pathogenic Messengers, Diagnostic Biomarkers, and Therapeutic Nanovectors.Pharmaceutics · 2026Review
- Exosomes Regulate Liver Diseases Through the TGF-β1/Smads Signaling Pathway and the Intervention of Traditional Chinese Medicine: A Narrative Review.Journal of inflammation research · 2026Review
- Angiotensin-Converting Enzyme Inhibitors to Prevent Liver Fibrosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: Scientific Speculation or an Opportunity to Improve Real Clinical Practice?International journal of molecular sciences · 2025Review
- Bone marrow mesenchymal stem cell-derived exosomes attenuate hepatic stellate cell activation through miR-223-3p-mediated mitophagy.BMC medical genomics · 2025Article
- Overexpression miR-125a-5p inhibits HSCs activation and alleviates liver fibrosis through TGF-β/Smad2/3 signaling pathway and autophagy.Cell death discovery · 2025Article
- Exosome-mediated Crosstalk in the Tumor Immune Microenvironment: Critical Drivers of Hepatocellular Carcinoma Progression.Journal of clinical and translational hepatology · 2025Review
- Dynamic crosstalk between HSCs and liver microenvironment: multicellular interactions in the regulation of liver fibrosis.Frontiers in cell and developmental biology · 2025Review
- Liver-derived Exosomal miRNA in NAFLD: Mechanisms of Action, Biomarkers, and Therapeutic Applications.Current medicinal chemistry · 2025Review
- Extracellular Vesicles in Viral Liver Diseases.Viruses · 2024Review
- MicroRNA-enriched exosome as dazzling dancer between cancer and immune cells.Journal of physiology and biochemistry · 2024Review
- Novel insights into the role of immunomodulatory extracellular vesicles in the pathogenesis of liver fibrosis.Biomarker research · 2024Review
- Large Extracellular Vesicles Derived from Natural Killer Cells Affect the Functions of Monocytes.International journal of molecular sciences · 2024Article
- Function and biomedical implications of exosomal microRNAs delivered by parenchymal and nonparenchymal cells in hepatocellular carcinoma.World journal of gastroenterology · 2023Review
- Interplays of liver fibrosis-associated microRNAs: Molecular mechanisms and implications in diagnosis and therapy.Genes & diseases · 2023Review
- The Important Roles of Natural Killer Cells in Liver Fibrosis.Biomedicines · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundActivation of hepatic stellate cells (HSCs) is a prominent driver of liver fibrosis. We previously demonstrated that exosomes derived from natural killer (NK) cells (NK-Exo) attenuated TGF-β1-induced HSC activation. Herein, this study was designed to investigate the mechanism underlying the action of NK-Exo.
methodsNK-Exo was isolated from NK-92MI cells and then administered into TGF-β1-treated LX-2 (human HSC line) cells. MiR-223 expression in NK-Exo was downregulated by transfecting NK-92MI cells with miR-223 inhibitor followed by exosome isolation. The HSC activation was evaluated by determining cell proliferation using CCK-8 assay and measuring the protein levels of α-SMA and CoL1A1 using western blot in LX-2 cells. The expression of miR-223 was detected by qRT-PCR. The interaction between miR-223 and ATG7 was analyzed by a dual-luciferase activity assay. The autophagy was evaluated by measuring the autophagy-related proteins using western blot.
resultsmiR-223 was highly expressed in NK-Exo and inhibition of miR-223 expression in NK-Exo abrogated the inhibitory effect of NK-Exo on TGF-β-induced HSC activation. ATG7 was confirmed as a direct target of miR-223. Furthermore, treatment with the autophagy activator rapamycin and ATG7 overexpression in LX-2 cells abolished the HSC activation-suppressive effect of NK-Exo.
conclusionNK-Exo attenuated TGF-β-induced HSC activation by transferring miR-223 that inhibited autophagy via targeting ATG7.
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