ArticleLaboratory investigation; a journal of technical methods and pathology2020
SPOCK1 overexpression induced by platelet-derived growth factor-BB promotes hepatic stellate cell activation and liver fibrosis through the integrin α5β1/PI3K/Akt signaling pathway.
Article in Laboratory investigation; a journal of technical methods and pathology, 2020. 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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31 citing papers in PubMed, 45 citations in OpenAlex.
- Intrahepatic Platelets Orchestrate Microenvironmental Remodelling and Cellular Crosstalk in Liver Fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Innovative analysis and future prospects of Bupleuri Radix's pharmacology and toxicity based on the gut-liver axis.MedScience · 2026Review
- SPOCK1 acts as a negative regulator of ferroptosis in non-small cell lung cancer.NPJ precision oncology · 2026Article
- Mechanism study of circCCDC134 regulating the biological behaviors of PDGF-BB-induced oral mucosal fibroblast.Scientific reports · 2026Article
- Human menstrual blood-derived stem cells secreted ECM1 directly interacts with LRP1α to ameliorate hepatic fibrosis through FoxO1 and mTOR signaling pathway.Stem cell research & therapy · 2025Article
- Association analysis of single nucleotide polymorphisms in the LIFR gene with lambing number in sheep.Frontiers in veterinary science · 2025Article
- Mechanistic insights into the therapeutic effects on liver fibrosis in Wilson's disease: a transcriptomic and network pharmacology-based approach.Frontiers in medicine · 2025Article
- SPOCK: Master regulator of malignant tumors (Review).Molecular medicine reports · 2024Review
- The possible pathogenesis of liver fibrosis: therapeutic potential of natural polyphenols.Pharmacological reports : PR · 2024Review
- From NAFLD to NASH: Understanding the spectrum of non-alcoholic liver diseases and their consequences.Heliyon · 2024Review
- Hypoxia-driven TNS4 fosters HNSCC tumorigenesis by stabilizing integrin α5β1 complex and triggering FAK-mediated Akt and TGFβ signaling pathways.International journal of biological sciences · 2024Article
- SLC41A1 overexpression correlates with immune cell infiltration in HCC and promotes its malignant progression.International journal of medical sciences · 2024Article
- The secreted neuronal signal Spock1 promotes blood-brain barrier development.Developmental cell · 2023Article
- Cell Adhesion Molecules in Fibrotic Diseases.Biomedicines · 2023Review
- Towards a Unified Approach in Autoimmune Fibrotic Signalling Pathways.International journal of molecular sciences · 2023Review
- Article
- Engineered fibrotic liver-targeted truncated transforming growth factor β receptor type II variant for superior anti-liver fibrosis therapy.Archives of pharmacal research · 2023Article
- N-Acetyl-L-cysteine facilitates tendon repair and promotes the tenogenic differentiation of tendon stem/progenitor cells by enhancing the integrin α5/β1/PI3K/AKT signaling.BMC molecular and cell biology · 2023Article
- Comprehensive Analysis of Sideroflexin 4 in Hepatocellular Carcinoma by Bioinformatics and Experiments.International journal of medical sciences · 2023Article
- The Pro-Fibrotic Response to Lens Injury Is Signaled in a PI3K Isoform-Specific Manner.Biomolecules · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
Sparc/osteonectin, cwcv, and kazal-like domain proteoglycan 1 (SPOCK1) is a matricellular protein which regulates cell proliferation, invasion, and survival but the function of SPOCK1 in liver fibrosis is obscure. In this study, we found that SPOCK1 expression increased significantly in fibrotic liver tissues and activated primary rat hepatic stellate cells (R-HSCs). SPOCK1 co-localized with α-smooth muscle actin (α-SMA) in the cytoplasm. Mechanistically, we found platelet-derived growth factor-BB (PDGF-BB) induced SPOCK1 expression by activating the PI3K/Akt/forkhead box M1 (FoxM1) signaling pathway. Intracellular SPOCK1 downregulation decreased the HSC activation, proliferation, and migration induced by PDGF-BB. Furthermore, intracellular SPOCK1 overexpression or recombinant SPOCK1 treatment promoted HSC activation, proliferation, and migration by activating the PI3K/Akt signaling pathway. Co-immunoprecipitation, double immunofluorescence staining indicated that SPOCK1 interacted with integrin α5β1, and neutralization of integrin α5β1 significantly reduced the role of recombinant SPOCK1 in HSCs. In vivo HSC-specific SPOCK1 knockdown following lentivirus administration dramatically ameliorated thioacetamide (TAA)-induced collagen deposition in rat livers. Collectively, our study indicates that SPOCK1 is crucial for hepatic fibrosis and it might be a promising therapeutic target.
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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.