ArticleInflammopharmacology2022
The anti-angiogenesis mechanism of Geniposide on rheumatoid arthritis is related to the regulation of PTEN.
Article in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Anti-arthritic and immunomodulatory effects of geniposide: a systematic review and meta-analysis of preclinical studies.Inflammopharmacology · 2025Pooled it
- Vanillic acid ameliorates collagen-induced arthritis by suppressing the inflammation response via inhibition of the MAPK and NF-κB signaling pathways.Inflammopharmacology · 2025Article
- The emerging role of vascular endothelial cell-mediated angiogenesis in the imbalance of RA synovial microenvironment and its clinical relevance.Frontiers in pharmacology · 2025Review
- PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024Review
- The protective effect of natural medicines in rheumatoid arthritis via inhibit angiogenesis.Frontiers in pharmacology · 2024Review
- LncRNA HOTAIR regulates the PI3K/AKT pathway via the miR-126-3p/PIK3R2 axis to participate in synovial angiogenesis in rheumatoid arthritis.Immunity, inflammation and disease · 2023Article
- Advances of the small molecule drugs regulating fibroblast-like synovial proliferation for rheumatoid arthritis.Frontiers in pharmacology · 2023Review
- Updated Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of Natural Product Geniposide.Molecules (Basel, Switzerland) · 2022Review
- Natural medicines of targeted rheumatoid arthritis and its action mechanism.Frontiers in immunology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Rheumatoid arthritis (RA) is a systemic immune disease characterized by joint inflammation and pannus. The nascent pannus contributes to synovial hyperplasia, cartilage, and tissue damage in RA. This study aims to explore the therapeutic effect and potential mechanism of Geniposide (GE) on RA angiogenesis, involving the participation of phosphate and tension homology deleted on chromosome ten (PTEN) and downstream pathways. Clinical manifestations, synovial pathomorphology, microvessel density, and the level of angiogenesis-related factors were used to evaluate the therapeutic effect of GE on adjuvant-induced arthritis (AA) rats. The proliferation, migration, and tube formation of human umbilical vein endothelial cells (HUVECs) indicate the degree of angiogenesis in vitro. Lentivirus over-expression of PTEN was employed to elucidate the potential mechanism. The results showed that GE improved the degree of arthritis and angiogenesis in AA rats. The expression of PTEN was decreased significantly in vivo and in vitro, and over-expression of PTEN improved the biological function of HUVECs to inhibit angiogenesis. GE inhibited the proliferation, migration, and tubule formation of HUVECs and plays an anti-angiogenesis role in vitro. Mechanism study showed that PTEN expression was increased and p-PI3K and p-Akt expression was decreased with GE treatment. It suggests that GE up-regulated the expression of PTEN and inhibited the activation of PI3K-Akt signal, which plays a role in inhibiting angiogenesis in RA in vivo and in vitro.
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