ArticleCell death & disease2018
Targeting of chondrocyte plasticity via connexin43 modulation attenuates cellular senescence and fosters a pro-regenerative environment in osteoarthritis.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
62 citing papers in PubMed, 98 citations in OpenAlex.
- Loss of connexin 43 in cartilage causes mitochondrial dysfunction and accelerates post-traumatic osteoarthritis progression.bioRxiv : the preprint server for biology · 2026Article
- Targeting cellular senescence in diabetic kidney disease: potential of regenerative, cell-based therapies and other senotherapeutic approaches.Kidney international · 2026Review
- Targeting mechanotransduction components as therapeutic strategies in osteoarthritis.Molecular biology reports · 2026Review
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- Nanoencapsulated senotherapeutic compounds targeting connexin-43 for enhanced wound healing.iScience · 2026Article
- Recent Advances in Therapeutic Approaches for Knee Osteoarthritis: a Narrative Review.Biomolecules & therapeutics · 2026Review
- Mitochondrial transplantation for osteoarthritis: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
- Nanotherapeutic Strategies for Osteoarthritis: Targeting Aging, Metabolism and Inflammation.International journal of nanomedicine · 2026Review
- Targeting the osteoimmune microenvironment to prevent regulated chondrocyte death in osteoarthritis: therapeutic potential of natural products.Frontiers in cell and developmental biology · 2026Review
- The osteoarthritis inflammatory ecosystem: a node-edge-boundary-emergent framework toward precision stratification and therapeutic hypothesis generation.Frontiers in medicine · 2026Review
- Aging microenvironment in osteoarthritis focusing on early-stage alterations and targeted therapies.Bone research · 2025Review
- Immunosenescence: signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Cx43 enhances response to BRAF/MEK inhibitors by reducing DNA repair capacity.Nature communications · 2025Article
- Cellular senescence in age-related musculoskeletal diseases.Frontiers of medicine · 2025Review
- Quercetin prevents the loss of chondrogenic capacity in expansion cultured human auricular chondrocytes by alleviating mitochondrial dysfunction.Regenerative therapy · 2025Article
- Osteoarthritis.Nature reviews. Disease primers · 2025Review
- Development and Characterization of Magnetic Nanoemulsion-Based Senolytic Peptides for Osteoarthritis Treatment.International journal of molecular sciences · 2025Article
- Article
- Cross-talk of inflammation and cellular senescence: a new insight into the occurrence and progression of osteoarthritis.Bone research · 2024Review
- Mesenchymal Stromal Cells for Aging Cartilage Regeneration: A Review.International journal of molecular sciences · 2024Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA), a chronic disease characterized by articular cartilage degeneration, is a leading cause of disability and pain worldwide. In OA, chondrocytes in cartilage undergo phenotypic changes and senescence, restricting cartilage regeneration and favouring disease progression. Similar to other wound-healing disorders, chondrocytes from OA patients show a chronic increase in the gap junction channel protein connexin43 (Cx43), which regulates signal transduction through the exchange of elements or recruitment/release of signalling factors. Although immature or stem-like cells are present in cartilage from OA patients, their origin and role in disease progression are unknown. In this study, we found that Cx43 acts as a positive regulator of chondrocyte-mesenchymal transition. Overactive Cx43 largely maintains the immature phenotype by increasing nuclear translocation of Twist-1 and tissue remodelling and proinflammatory agents, such as MMPs and IL-1β, which in turn cause cellular senescence through upregulation of p53, p16
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Registered trials
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.