ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2023
Nuclear protein-1 is the common link for pathways activated by aging and obesity in chondrocytes: A potential therapeutic target for osteoarthritis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Human umbilical cord mesenchymal stem cells alleviate colon epithelial apoptosis in ulcerative colitis by activating inositol-requiring enzyme 1/X-box binding protein 1 signaling.Stem cells translational medicine · 2026Article
- Nuclear protein 1 protects against neonatal hypoxic-ischemic encephalopathy by inhibiting neuronal ferroptosis by improving iron storage.In vitro cellular & developmental biology. Animal · 2025Article
- Comparative Analysis of the Therapeutic Potential of Extracellular Vesicles Secreted by Aged and Young Bone Marrow-Derived Mesenchymal Stem Cells in Osteoarthritis Pathogenesis.Cell proliferation · 2025Article
- Potential Roles of Long Non-coding RNAs in the Pathogenesis of Periodontitis: Inflammation Response, Immune Infiltration, Collagen Fibers Synthesis, and Bone Remodeling.Current medicinal chemistry · 2025Article
- Association of organs-crosstalk with the pathogenesis of osteoarthritis: cartilage as a key player.Frontiers in endocrinology · 2025Review
- The Bidirectional Role of Obesity and Aging in the Pathogenesis of Osteoarthritis: Molecular Mechanisms, Epigenetic Insights, and Therapeutic Implications.Journal of inflammation research · 2025Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Pathways leading to osteoarthritis (OA) are diverse depending on the risk factors involved; thus, developing OA therapeutics has been challenging. Here we report that nuclear protein-1 (Nupr1), a stress-inducible protein/transcription factor, is activated by pathways associated with obesity and aging in chondrocytes. Treatment of human chondrocytes with free fatty acids (palmitate and oleate; a model for high-fat diet/obesity) induced PERK signaling and increased expression of caspase-3, TRB3, and Nupr1. On the other hand, treatment of chondrocytes with menadione (oxidative stress inducer) induced oxidation of IRE1, activated antioxidant response (higher Nrf2 expression), and increased expression of Nupr1 and matrix metalloproteinases. Experimental OA was induced by destabilization of the medial meniscus (DMM) in the knee joints of Nupr1
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