ArticleCell death & disease2017
Interaction between autophagy and senescence is required for dihydroartemisinin to alleviate liver fibrosis.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 95 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Dual Roles of Autophagy in Endometrial Fibrosis and Its Implications in Age-Related Reproductive Dysfunction.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Hydrogen sulfide regulation in redox homeostasis and programmed cell death: mechanistic insights and implications in cancer.Journal of advanced research · 2026Review
- [Research progress on cellular senescence and liver diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- <p>Beyond hepatic stellate cell heterogeneity: Resolving fibrosis, restoring regeneration (Review)</p>.International journal of molecular medicine · 2026Review
- Dihydroartemisinin: A Promising Therapeutic Agent Against the Hepatitis-to-Hepatocellular Carcinoma Cascade.Drug design, development and therapy · 2025Review
- Guts for Self-Eating: Role of Autophagy in Gastrointestinal Health and Disease.Gastro hep advances · 2025Review
- The cell fate regulator DACH1 modulates ferroptosis through affecting P53/SLC25A37 signaling in fibrotic disease.Hepatology communications · 2024Article
- Advances in Research on the Effectiveness and Mechanism of Active Ingredients from Traditional Chinese Medicine in Regulating Hepatic Stellate Cells Autophagy Against Hepatic Fibrosis.Drug design, development and therapy · 2024Review
- Dihydroartemisinin inhibits the activation and proliferation of hepatic stellate cells by regulating miR‑29b‑3p.International journal of molecular medicine · 2023Article
- Autophagy in intestinal fibrosis: relevance in inflammatory bowel disease.Frontiers in pharmacology · 2023Review
- Dihydroartemisinin suppresses renal fibrosis in mice by inhibiting DNA-methyltransferase 1 and increasing Klotho.Acta pharmacologica Sinica · 2022Article
- 18beta-glycyrrhetinic acid induces ROS-mediated apoptosis to ameliorate hepatic fibrosis by targeting PRDX1/2 in activated HSCs.Journal of pharmaceutical analysis · 2022Article
- High TRB3 expression induces chondrocyte autophagy and senescence in osteoarthritis cartilage.Aging · 2022Article
- Celastrol induces ferroptosis in activated HSCs to ameliorate hepatic fibrosisActa pharmaceutica Sinica. B · 2022Article
- Why Senescent Cells Are Resistant to Apoptosis: An Insight for Senolytic Development.Frontiers in cell and developmental biology · 2022Review
- Dihydroartemisinin Exerts Antifibrotic and Anti-Inflammatory Effects in Graves' Ophthalmopathy by Targeting Orbital Fibroblasts.Frontiers in endocrinology · 2022Article
- Article
- High-Mobility Group AT-Hook 1 Served as a Prognosis Biomarker and Associated with Immune Infiltrate in Hepatocellular Carcinoma.International journal of general medicine · 2022Article
- Dihydroartemisinin alleviates skin fibrosis and endothelial dysfunction in bleomycin-induced skin fibrosis models.Clinical rheumatology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy and cellular senescence are stress responses essential for homeostasis. Therefore, they may represent new pharmacologic targets for drug development to treat diseases. In this study, we sought to evaluate the effect of dihydroartemisinin (DHA) on senescence of activated hepatic stellate cells (HSCs), and to further elucidate the underlying mechanisms. We found that DHA treatment induced the accumulation of senescent activated HSCs in rat fibrotic liver, and promoted the expression of senescence markers p53, p16, p21 and Hmga1 in cell model. Importantly, our study identified the transcription factor GATA6 as an upstream molecule in the facilitation of DHA-induced HSC senescence. GATA6 accumulation promoted DHA-induced p53 and p16 upregulation, and contributed to HSC senescence. By contrast, siRNA-mediated knockdown of GATA6 dramatically abolished DHA-induced upregulation of p53 and p16, and in turn inhibited HSC senescence. Interestingly, DHA also appeared to increase autophagosome generation and autophagic flux in activated HSCs, which was underlying mechanism for DHA-induced GATA6 accumulation. Autophagy depletion impaired GATA6 accumulation, while autophagy induction showed a synergistic effect with DHA. Attractively, p62 was found to act as a negative regulator of GATA6 accumulation. Treatment of cultured HSCs with various autophagy inhibitors, led to an inhibition of DHA-induced p62 degradation, and in turn, prevented DHA-induced GATA6 accumulation and HSC senescence. Overall, these results provide novel implications to reveal the molecular mechanism of DHA-induced senescence, by which points to the possibility of using DHA based proautophagic drugs for the treatment of liver fibrosis.
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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.