ArticleThe Journal of biological chemistry2011
Delta-like 1 serves as a new target and contributor to liver fibrosis down-regulated by mesenchymal stem cell transplantation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- Inhibition of DLK1 regulates AT2 differentiation and alleviates established pulmonary fibrosis by upregulating TTF-1/CLDN6.Respiratory research · 2025Article
- Pericardial delta like non-canonical NOTCH ligand 1 (Dlk1) augments fibrosis in the heart through epithelial to mesenchymal transition.Clinical and translational medicine · 2024Article
- DLK1 overexpression improves sepsis-induced cardiac dysfunction and fibrosis in mice through the TGF-β1/Smad3 signaling pathway and MMPs.Journal of molecular histology · 2023Article
- Multiple Dimensions of using Mesenchymal Stem Cells for Treating Liver Diseases: From Bench to Beside.Stem cell reviews and reports · 2023Review
- Umbilical cord mesenchymal stem cells relieve osteoarthritis in rats through immunoregulation and inhibition of chondrocyte apoptosis.Scientific reports · 2023Article
- TGFβJournal of cellular and molecular medicine · 2023Article
- The Effects of Programmed Cell Death of Mesenchymal Stem Cells on the Development of Liver Fibrosis.Stem cells international · 2023Review
- Targeting FAPα-expressing hepatic stellate cells overcomes resistance to antiangiogenics in colorectal cancer liver metastasis models.The Journal of clinical investigation · 2022Article
- Pituitary Tumor-Transforming Gene 1/Delta like Non-Canonical Notch Ligand 1 Signaling in Chronic Liver Diseases.International journal of molecular sciences · 2022Review
- The pituitary tumour-transforming gene 1/delta-like homologue 1 pathway plays a key role in liver fibrogenesis.Liver international : official journal of the International Association for the Study of the Liver · 2022Article
- Stem Cell-based Therapy Strategy for Hepatic Fibrosis by Targeting Intrahepatic Cells.Stem cell reviews and reports · 2022Review
- Mesenchymal stem cells attenuate liver fibrosis by targeting Ly6CCell death discovery · 2021Article
- Mesenchymal stem cell-based treatment in autoimmune liver diseases: underlying roles, advantages and challenges.Therapeutic advances in chronic disease · 2021Review
- Human umbilical cord mesenchymal stem cells ameliorate liver fibrosisWorld journal of stem cells · 2019Review
- Bone marrow mesenchymal stem cells attenuate the progression of focal segmental glomerulosclerosis in rat models.BMC nephrology · 2018Article
- Delta-like 2 negatively regulates chondrogenic differentiation.Journal of cellular physiology · 2018Article
- Human umbilical cord mesenchymal stem cells inhibit proliferation of hepatic stellate cells in vitro.International journal of molecular medicine · 2018Article
- Identification of DEAD-Box RNA Helicase DDX41 as a Trafficking Protein That Involves in Multiple Innate Immune Signaling Pathways in a Zebrafish Model.Frontiers in immunology · 2018Article
- Umbilical cord blood stem cells transplantation as an adjunctive treatment strategy for liver cirrhosis in Chinese population: a meta-analysis of effectiveness and safety.Therapeutics and clinical risk management · 2018Article
- Smad7-overexpressing rat BMSCs inhibit the fibrosis of hepatic stellate cells by regulating the TGF-β1/Smad signaling pathway.Experimental and therapeutic medicine · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic liver injury always progresses to fibrosis and eventually to cirrhosis, a massive health care burden worldwide. Delta-like 1 (Dlk1) is well known as an inhibitor of adipocyte differentiation. However, whether it is involved in liver fibrosis remains unclear. Here, we provide the first evidence that Dlk1 is a critical contributor to liver fibrosis through promoting activation of hepatic stellate cells (HSCs) during chronic liver injury. We found that upon liver injury, Dlk1 was dramatically induced and initially expressed in hepatocytes and then into the HSCs by a paracrine manner. It leads to the activation of HSCs, which is considered to be a pivotal event in liver fibrogenesis. Two forms (∼50 and ∼25 kDa) of the Dlk1 protein were detected by Western blot analysis. In vitro administration of Dlk1 significantly promoted HSC activation, whereas in vivo knockdown of Dlk1 dramatically inhibited HSC activation and the subsequent fibrosis. The large soluble form (∼50 kDa) of Dlk1 was shown to contribute to HSC activation. We were encouraged to find the Dlk1-promoted HSC activation and liver fibrosis can be depressed by transplantation of bone marrow-mesenchymal stem cells (BM-MSCs). Furthermore, we demonstrated that FGF2 was up-regulated in BM-MSCs under injury stimulation, and it probably participated in the inhibition of Dlk1 by BM-MSCs. Our findings provide a novel role of Dlk1 in liver fibrosis leading to a better understanding of the molecular basis in fibrosis and cirrhosis and also give insights into the cellular and molecular mechanisms of MSC biology in liver repair.
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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.