The DOI matches its Crossref record; 125 of the 130 references it cites were found in a registry or an index.
Aging and osteoarthritis: the role of chondrocyte senescence and aging changes in the cartilage matrix
Open accessAbstract
Objective Age-related changes in multiple components of the musculoskeletal system may contribute to the well established link between aging and osteoarthritis (OA). This review focused on potential mechanisms by which age-related changes in the articular cartilage could contribute to the development of OA.Methods The peer-reviewed literature published prior to February 2009 in the PubMed database was searched using pre-defined search criteria. Articles, selected for their relevance to aging and articular chondrocytes or cartilage, were summarized.Results Articular chondrocytes exhibit an age-related decline in proliferative and synthetic capacity while maintaining the ability to produce pro-inflammatory mediators and matrix degrading enzymes. These findings are characteristic of the senescent secretory phenotype and are most likely a consequence of extrinsic stress-induced senescence driven by oxidative stress rather than intrinsic replicative senescence. Extracellular matrix changes with aging also contribute to the propensity to develop OA and include the accumulation of proteins modified by non-enzymatic glycation.Conclusion The effects of aging on chondrocytes and their matrix result in a tissue that is less able to maintain homeostasis when stressed, resulting in breakdown and loss of the articular cartilage, a hallmark of OA. A better understanding of the basic mechanisms underlying senescence and how the process may be modified could provide novel ways to slow the development of OA.
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“the age-related decline in the proliferative and synthetic capacities of articular chondrocytes may reduce subsequent tissue regeneration33.”
From Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment (2017) · cites this paper as [33]
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“These findings suggest that UBX0101 can clear SnCs from aged articular cartilage, but the age-related decline in the proliferative and synthetic capacities of articular chondrocytes may reduce subsequent tissue regeneration33.”
From Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment (2017) · cites this paper as [33]
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Metadata
- Authors
- Loeser, R. F.
- Affiliations
- Wake Forest University Health Sciences (US)
- Corresponding author
- Loeser, R.F.
- ORCID
- Loeser, R.F.
- Venue
- Osteoarthritis and Cartilage
- Publisher
- Elsevier BV
- Published
- 2009-08
- Volume
- 17
- Issue
- 8
- Pages
- 971-979
- ISSN
- 1063-4584 (ISSN-L)
- PMC
- PMC2713363
- OpenAlex
- W2025243746
- Cited by
- 726
- References
- 130
- Citations by year
- 2026: 39 · 2025: 55 · 2024: 48 · 2023: 51 · 2022: 39 · 2021: 75 · 2020: 57 · 2019: 48 · 2018: 35 · 2017: 46 · 2016: 43 · 2015: 49 · 2014: 36 · 2013: 29 · 2012: 27
- FWCI
- 3.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Osteoarthritis and Cartilage (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG016697, R01-AG-16697, P30AG021332)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR49003, R01AR049003)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Keywords
- osteoarthritis, aging, chondrocyte senescence, articular cartilage, oxidative stress, replicative senescence, extracellular matrix, glycation, pro-inflammatory mediators, matrix-degrading enzymes, cartilage homeostasis
- MeSH terms
- Aging, Animals, Cartilage, Articular, Humans, Osteoarthritis, Oxidative Stress, Chondrocytes
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