Mechanisms and therapeutic implications of cellular senescence in osteoarthritis
Open accessAbstract
The development of osteoarthritis (OA) correlates with a rise in the number of senescent cells in joint tissues, and the senescence-associated secretory phenotype (SASP) has been implicated in cartilage degradation and OA. Age-related mitochondrial dysfunction and associated oxidative stress might induce senescence in joint tissue cells. However, senescence is not the only driver of OA, and the mechanisms by which senescent cells contribute to disease progression are not fully understood. Furthermore, it remains uncertain which joint cells and SASP-factors contribute to the OA phenotype. Research in the field has looked at developing therapeutics (namely senolytics and senomorphics) that eliminate or alter senescent cells to stop disease progression and pathogenesis. A better understanding of how senescence contributes to joint dysfunction may enhance the effectiveness of these approaches and provide relief for patients with OA.
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Chondrocytes in articular cartilage from osteoarthritis show senescence markers including DDR activation.
“Chondrocytes, the cells that constitute the articular cartilage, show several senescence markers, including DDR activation, in osteoarthritis119,120.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [120]
The ‘Cellular senescence and OA’ section reports senescent signatures in chondrocytes derived from osteoarthritic cartilage, and the ‘Extracellular vesicles’ section reports more senescent chondrocytes in OA cartilage than in healthy cartilage. However, the paper does not identify DDR activation as a marker observed in those chondrocytes; its discussion of DNA damage as a senescence trigger does not establish that specific point. (LLM, conf=0.85)
Experimental — accuracy not yet measuredTissue ageing is caused by the accumulation of senescent cells, which alters physiological responses in the surrounding microenvironment in an autocrine and paracrine fashion through SASP.
“Over the past decade, it has become clear that tissue ageing is caused by the accumulation of senescent cells, which alters the physiological responses in the surrounding microenvironment in an autocrine and paracrine fashion through SASP.2,3”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [3]
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References 127 · Cited by 761
Research works printed but not linked: 4
- [98]US National Library of Medicine. ClinicalTrials.gov https://clinicaltrials.gov/ct2/show/NCT04229225 (2020). 28792816
- [99]US National Library of Medicine. ClinicalTrials.gov https://clinicaltrials.gov/ct2/show/NCT04349956 (2020). 28792816
- [105]US National Library of Medicine. ClinicalTrials.gov https://clinicaltrials.gov/ct2/show/NCT04210986 (2020). 28792816
- [124]US National Library of Medicine. ClinicalTrials.gov https://clinicaltrials.gov/ct2/show/NCT02477059 (2019). 28792816
- Authors
- Coryell, P. R., Diekman, B. O., & Loeser, R. F.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Loeser, Richard F.
- Venue
- Nature Reviews Rheumatology
- Published
- 2020-11-18
- Volume
- 17
- Issue
- 1
- Pages
- 47-57
- ISSN
- 1759-4790 (ISSN-L)
- 1759-4804
- PMC
- PMC8035495
- OpenAlex
- W3101423962
- Cited by
- 761
- References
- 127
- Citations by year
- 2026: 139 · 2025: 177 · 2024: 174 · 2023: 125 · 2022: 94 · 2021: 52
- FWCI
- 10.54
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Reviews Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG044034)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R37AR049003)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- osteoarthritis, cellular senescence, senescence-associated secretory phenotype, cartilage degeneration, mitochondrial dysfunction, oxidative stress, senolytics, senomorphics, senescent cells, joint tissue, disease progression
- MeSH terms
- Aging, Animals, Hypolipidemic Agents, Cartilage, Articular, Clinical Trials as Topic, DNA Damage, Humans, Osteoarthritis, Phenotype, Biomarkers, Cellular Senescence, Oxidative Stress, Disease Progression, Chondrocytes, Models, Animal, Protein Kinase Inhibitors, Mice, TOR Serine-Threonine Kinases, Antibodies, Monoclonal, Humanized, Ageism
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