ArticleBioMed research international2015
Pim-2/mTORC1 Pathway Shapes Inflammatory Capacity in Rheumatoid Arthritis Synovial Cells Exposed to Lipid Peroxidations.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Application of stem cell-derived exosomes in bone and joint diseases: Recent advances enabled by diverse carrier technologies.World journal of stem cells · 2025Review
- Rapamycin reveals neuropeptide Y as a regulator of senescence and inflammatory pathways in arthritis.Neuropeptides · 2025Article
- The Therapeutic Potential of Phytochemicals Unlocks New Avenues in the Management of Rheumatoid Arthritis.International journal of molecular sciences · 2025Review
- PIM Kinases as Potential Biomarkers and Therapeutic Targets in Inflammatory Arthritides.International journal of molecular sciences · 2024Article
- Regulation of cagA-Helicobacter on gastric PIM2 expression in gastric cancer.Cancer biomarkers : section A of Disease markers · 2024Article
- Protective effects of cell permeable Tat-PIM2 protein on oxidative stress induced dopaminergic neuronal cell death.Heliyon · 2023Article
- Role of PIM2 in acute lung injury induced by sepsis.Experimental and therapeutic medicine · 2022Article
- Pim-2 kinase inhibits inflammation by suppressing the mTORC1 pathway in atherosclerosis.Aging · 2021Article
- Article
- Role of PIM2 in allergic asthma.Molecular medicine reports · 2017Article
- Identification of Palmitoleic Acid Controlled by mTOR Signaling as a Biomarker of Polymyositis.Journal of immunology research · 2017Article
- DEPTOR-mTOR Signaling Is Critical for Lipid Metabolism and Inflammation Homeostasis of Lymphocytes in Human PBMC Culture.Journal of immunology research · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis is a systemic autoimmune disease characterized by chronic inflammation of multiple joints, with disruption of joint cartilage. The proliferation of synovial fibroblasts in response to multiple inflammation factors is central to the pathogenesis of rheumatoid arthritis. Our previous studies showed that 4-HNE may induce synovial intrinsic inflammations by activating NF-κB pathways and lead to cell apoptosis. However, the molecular mechanisms of how synovial NF-κB activation is modulated are not fully understood. Here, the present findings demonstrated that 4-HNE may induce synovial intrinsic inflammations by mTORC1 inactivation. While ectopic activation of mTORC1 pathway by the overexpression of Pim-2 may disrupt the initiation of inflammatory reactions and maintain synovial homeostasis, our findings will help to uncover novel signaling pathways between inflammations and oxidative stress in rheumatoid arthritis development and imply that Pim-2/mTORC1 pathway may be critical for the initiation of inflammatory reactions in human rheumatoid arthritis synovial cells.
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