ArticleArthritis research & therapy2014
p16INK4a and its regulator miR-24 link senescence and chondrocyte terminal differentiation-associated matrix remodeling in osteoarthritis.
Article in Arthritis research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 2 of them syntheses that pooled it.
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Who cites it
135 citing papers in PubMed, 2 syntheses or guidelines pooled it, 215 citations in OpenAlex.
- Telomere length in patients with osteoarthritis: a systematic review and meta-analysis.Aging clinical and experimental research · 2022Pooled it
- An Evidence-Based Systematic Review of Human Knee Post-Traumatic Osteoarthritis (PTOA): Timeline of Clinical Presentation and Disease Markers, Comparison of Knee Joint PTOA Models and Early Disease Implications.International journal of molecular sciences · 2021Pooled it
- Pharmacological targeting of the senescence-associated secretory phenotype in atherosclerosis: therapeutic potential of senolytics and senomorphics.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Cartilage targeted grape skin-derived extracellular vesicles ameliorate osteoarthritis by attenuating chondrocyte senescence.Journal of nanobiotechnology · 2026Article
- Biomarkers of Inflammaging and Cellular Senescence in Musculoskeletal (MSK) Diseases: The Knowns and the Unknowns.Biomedicines · 2026Article
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- Senescent cells in systemic aging: SASP heterogeneity, immune escape, and endocrine modulation.Biogerontology · 2026Review
- The ganglioside GD3 and its synthase (ST8SIA1) as novel senescence markers associated with osteoarthritis.GeroScience · 2026Article
- Endothelial Dysfunction Contributes to Chondrocyte Senescence Associated With Insulin-Like Growth Factor-Binding Protein-6 in a Spontaneously Hypertensive Rat Model.Journal of the American Heart Association · 2026Article
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- Impact of flow cytometry-based sorting on microRNA signature of extracellular vesicles derived from mesenchymal stromal cells: a proof-of-concept study.Extracellular vesicles and circulating nucleic acids · 2026Article
- MicroRNA-mediated mechanotransduction and chondrocyte differentiation in mesenchymal stem cells.Animal cells and systems · 2026Review
- Lactate-driven lactylation reprograms chondrocyte fate and joint inflammation in osteoarthritis: linking metabolism with epigenetic regulation.Frontiers in cell and developmental biology · 2026Review
- The Impact of Senescence-Associated Secretory Phenotype (SASP) on Head and Neck Cancers: From Biology to Therapy.Cancers · 2025Review
- Exploring senescence markers as potential drivers of osteoarthritis pain in aging adults.Experimental gerontology · 2025Review
- Biomarkers of aging as it relates osteoarthritis: we can't improve what we can't measure.Connective tissue research · 2025Review
- 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
- The intersection of aging and estrogen in osteoarthritis.npj women's health · 2025Review
- Comparative analysis of adipose-, bone marrow-, and amniotic membrane-derived MSC secretomes and EVs reveals shared and source-specific therapeutic signatures for osteoarthritis.Extracellular vesicles and circulating nucleic acids · 2025Article
- Article
75 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionRecent evidence suggests that tissue accumulation of senescent p16INK4a-positive cells during the life span would be deleterious for tissue functions and could be the consequence of inherent age-associated disorders. Osteoarthritis (OA) is characterized by the accumulation of chondrocytes expressing p16INK4a and markers of the senescence-associated secretory phenotype (SASP), including the matrix remodeling metalloproteases MMP1/MMP13 and pro-inflammatory cytokines interleukin-8 (IL-8) and IL-6. Here, we evaluated the role of p16INK4a in the OA-induced SASP and its regulation by microRNAs (miRs).
methodsWe used IL-1-beta-treated primary OA chondrocytes cultured in three-dimensional setting or mesenchymal stem cells differentiated into chondrocyte to follow p16INK4a expression. By transient transfection experiments and the use of knockout mice, we validate p16INK4a function in chondrocytes and its regulation by one miR identified by means of a genome-wide miR-array analysis.
resultsp16INK4a is induced upon IL-1-beta treatment and also during in vitro chondrogenesis. In the mouse model, Ink4a locus favors in vivo the proportion of terminally differentiated chondrocytes. When overexpressed in chondrocytes, p16INK4a is sufficient to induce the production of the two matrix remodeling enzymes, MMP1 and MMP13, thus linking senescence with OA pathogenesis and bone development. We identified miR-24 as a negative regulator of p16INK4a. Accordingly, p16INK4a expression increased while miR-24 level was repressed upon IL-1-beta addition, in OA cartilage and during in vitro terminal chondrogenesis.
conclusionsWe disclosed herein a new role of the senescence marker p16INK4a and its regulation by miR-24 during OA and terminal chondrogenesis.
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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.