ArticleArthritis research & therapy2013
Linked decreases in liver kinase B1 and AMP-activated protein kinase activity modulate matrix catabolic responses to biomechanical injury in chondrocytes.
Article in Arthritis research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Meta-analysis Integrated With Multi-omics Data Analysis to Elucidate Pathogenic Mechanisms of Age-Related Knee Osteoarthritis in Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Pooled it
- Ceritinib induces ferroptosis via TRIM21-mediated GLUT1 ubiquitination and AMPK-driven metabolic reprogramming in breast cancer.iScience · 2026Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Dapagliflozin regulates chondrocyte homeostasis and protects against osteoarthritis via targets AMPKα and SGLT2.Cell death discovery · 2026Article
- Accelerated cartilage regeneration via chondrocyte metabolic reprogramming using nano-steroid-conjugated mesenchymal stem cells in osteoarthritis.Theranostics · 2026Article
- Increased TNN in Knee Osteoarthritis Accelerates Cartilage Damage via the Negative Regulation of AMPK-PPARγ Signalling.Journal of cellular and molecular medicine · 2025Article
- Detumescence Analgesic Plaster mitigates knee osteoarthritis via active ingredients targeting mitochondrial complex 1/AMPK/MYL3-regulated cartilage homeostasis.Chinese medicine · 2025Article
- Follow the Molecule from Crystal Arthropathy to Comorbidities: The 2024 G-CAN Gold Medal Award Awardee Lecture.Gout, urate, and crystal deposition disease · 2025Article
- Targeting TREM-1 receptors with metformin and pravastatin modulate monosodium iodoacetate-induced osteoarthritis.Inflammopharmacology · 2025Article
- Metabolic Reprogramming in Stromal and Immune Cells in Rheumatoid Arthritis and Osteoarthritis: Therapeutic Possibilities.European journal of immunology · 2025Review
- Development of novel osteoarthritis therapy by targeting AMPK-β-catenin-Runx2 signaling.Genes & diseases · 2025Review
- AMPK signaling in osteoarthritis: from mechanisms to targeted therapeutics.Frontiers in pharmacology · 2025Review
- Recent development of mitochondrial metabolism and dysfunction in osteoarthritis.Frontiers in pharmacology · 2025Review
- Modulating Autophagy in Osteoarthritis: Exploring Emerging Therapeutic Drug Targets.International journal of molecular sciences · 2024Review
- β-Hydroxybutyrate enhances chondrocyte mitophagy and reduces cartilage degeneration in osteoarthritis via the HCAR2/AMPK/PINK1/Parkin pathway.Aging cell · 2024Article
- The involvement of signaling pathways in the pathogenesis of osteoarthritis: An update.Journal of orthopaedic translation · 2024Review
- Advances in the study of mitophagy in osteoarthritis.Journal of Zhejiang University. Science. B · 2024Article
- Effects of glucose concentration and oxygen partial pressure on the respiratory metabolism of sheep temporomandibular joint disc cells.Experimental and therapeutic medicine · 2023Article
- Enpp1 deficiency caused chondrocyte apoptosis by inhibiting AMPK signaling pathway.Journal of orthopaedic surgery and research · 2023Article
- Adenosine A2A receptor activation reduces chondrocyte senescence.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
2 more citing papers are in PubMed but not listed here.
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6 authors at 5 institutions in 1 country.
Funding
Abstract
introductionAMP-activated protein kinase (AMPK) maintains cultured chondrocyte matrix homeostasis in response to inflammatory cytokines. AMPK activity is decreased in human knee osteoarthritis (OA) chondrocytes. Liver kinase B1 (LKB1) is one of the upstream activators of AMPK. Hence, we examined the relationship between LKB1 and AMPK activity in OA and aging cartilages, and in chondrocytes subjected to inflammatory cytokine treatment and biomechanical compression injury, and performed translational studies of AMPK pharmacologic activation.
methodsWe assessed activity (phosphorylation) of LKB1 and AMPKα in mouse knee OA cartilage, in aging mouse cartilage (6 to 24 months), and in chondrocytes after mechanical injury by dynamic compression, via immunohistochemistry or western blot. We knocked down LKB1 by siRNA transfection. Nitric oxide, matrix metalloproteinase (MMP)-3, and MMP-13 release were measured by Griess reaction and ELISA, respectively.
resultsKnockdown of LKB1 attenuated chondrocyte AMPK activity, and increased nitric oxide, MMP-3 and MMP-13 release (P <0.05) in response to IL-1β and TNFα. Both LKB1 and AMPK activity were decreased in mouse knee OA and aged knee cartilage, and in bovine chondrocytes after biomechanical injury. Pretreatment of bovine chondrocytes with AMPK activators AICAR and A-769662 inhibited both AMPKα dephosphorylation and catabolic responses after biomechanical injury.
conclusionLKB1 is required for chondrocyte AMPK activity, thereby inhibiting matrix catabolic responses to inflammatory cytokines. Concurrent loss of LKB1 and AMPK activity in articular chondrocytes is associated with OA, aging and biomechanical injury. Conversely, pharmacologic AMPK activation attenuates catabolic responses to biomechanical injury, suggesting a potentially novel approach to inhibit OA development and progression.
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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.