ArticleJournal of advanced research2025
TRPM2-mediated feed-forward loop promotes chondrocyte damage in osteoarthritis via calcium-cGAS-STING-NF-κB pathway.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Analgesic effects of different administration routes of non-steroidal anti-inflammatory drugs in orthopedic postoperative pain management: a meta-analysis based on randomized controlled trials.Journal of orthopaedic surgery and research · 2026Pooled it
- Aerobic Exercise Mitigates Experimental Knee Osteoarthritis via Inhibition of cGAS-STING Signaling.Microbiology and immunology · 2026Article
- Mechanism of RORα in promoting osteoarthritis through p53 deubiquitination-mediated chondrocyte ferroptosis.iScience · 2026Article
- Ectoine Inhibits IL-1β-Induced Inflammation by Suppressing the NF-κB Pathway in Chondrocytes and Alleviates Osteoarthritis in a Rat Model.Biomedicines · 2026Article
- USP7 Regulates TRPV1 Deubiquitination to Mediate Chondrocyte Ferroptosis and Alleviate Osteoarthritis.The Kaohsiung journal of medical sciences · 2026Article
- [Protective effect and mechanism of TSPAN9-mediated mitocytosis in interleukin-1β-induced rat chondrocyte senescence].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- cGAS-STING/HMGB1-mediated senescence induced by LRRK2 accelerates cartilage degeneration in osteoarthritis.Cell death & disease · 2026Article
- TRPM2 couples cell-autonomous type-I interferon signaling to pigmentation homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Photothermal reprogramming of synovial M1 macrophages reshapes the pro-inflammatory microenvironment to reverse temporomandibular joint osteoarthritis.Journal of nanobiotechnology · 2026Article
- Review
- Targeting the mitochondrial metabolite-dynamics-MDVs-MitoEVs axis: a new frontier in osteoarthritis management.Journal of translational medicine · 2026Review
- Pathogenic Implications of the THY1/NF-κB Feedback Relationship in Osteoarthritis and Its Potential as a Therapeutic Target.Journal of inflammation research · 2026Article
- Mitochondrial 8-Oxoguanine DNA Glycosylase 1-Mitochondrial Permeability Transition Pore Axis Drives Mitochondrial DNA Escape and Accelerates Osteoarthritis Progression.Research (Washington, D.C.) · 2026Article
- From mechanical adaptation to innate immune reprogramming in osteoarthritis: a load-immunity framework.Frontiers in immunology · 2026Review
- Bimetallic Copper-Manganese Zeolitic Imidazolate Framework Nanozyme Scavenges Reactive Oxygen Species to Alleviate Osteoarthritis via Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Axis and Autophagic Flux Restoration.Biomaterials research · 2026Article
- Revisiting osteoarthritis pathogenesis through the lens of cGAS-STING: Mitochondrial damage, pyroptosis, and inflammatory cascades.Journal of orthopaedic translation · 2026Review
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- METTL3 promotes chondrocyte injury in osteoarthritis by increasing CTSB expression.Journal of orthopaedic surgery and research · 2025Article
- EXO/hydrogel system for sequential regulation of endogenous hyaline cartilage regeneration.Materials today. Bio · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionsOsteoarthritis (OA) is a significant contributor to disability in the elderly population. However, current therapeutic options are limited. The transient receptor potential melastatin 2 (TRPM2) is involved in a range of disease processes, yet its role in OA remains unclear.
objectivesTo investigate the role of TRPM2 in OA.
methodsCartilage samples were collected from patients with osteoarthritis (OA) and mice with OA to examine TRPM2 expression levels. To investigate the effects of TRPM2 modulation on the destabilization of the medial meniscus (DMM) induced knee OA in mice, we utilized TRPM2 knockout mice and employed adenovirus-mediated overexpression of TRPM2. Furthermore, siRNA-mediated TRPM2 knockdown or plasmid-mediated TRPM2 overexpression was conducted to explore the role of TRPM2 in IL-1β-induced chondrocytes. The regulatory mechanism of IL-1β on TRPM2 expression was screened by signaling pathway inhibitors, and the transcription factors and binding sites of TRPM2 were predicted using the database. The binding of RELA (NF-κB-p65) to the Trpm2 promoter was verified by chip-PCR and ChIP-qPCR. The therapeutic potential of Ca
resultsAn increased expression of TRPM2 was observed in the cartilage of OA patients and OA mice. Furthermore, mice deficient in Trpm2 exhibited a protective effect against DMM-induced OA progression. In contrast, TRPM2 overexpression resulted in exacerbation of DMM-induced OA and thepromotion of an OA-like phenotype of chondrocytes. TRPM2 was upregulated by IL-1β in an NF-κB-p65-dependent manner. Subsequently, the TRPM2-Ca
conclusionsOur data collectively revealed a pathological feedback loop involving TRPM2, Ca
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