Events in articular chondrocytes with aging

Daniel J. Leong, Hui (Herb) Sun

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

It is well accepted that aging is one of the most prominent risk factors for the initiation and progression of osteoarthritis. One of the most pronounced age-related changes in chondrocytes is the exhibition of a senescent phenotype, which is the result of several factors including the accumulation of reactive oxygen species and advanced glycation end products. Compared with a normal chondrocyte, senescent chondrocytes exhibit an impaired ability to respond to many mechanical and inflammatory insults to the articular cartilage. Furthermore, protein secretion is altered in aging chondrocytes, demonstrated by a decrease in anabolic activity and increased production of proinflammatory cytokines and matrix-degrading enzymes. Together, these events may make the articular cartilage matrix more susceptible to damage and lead to the onset of osteoarthritis. A better understanding of the mechanisms underlying age-related chondrocyte pathophysiology may be critical for the development of novel therapeutic interventions for progressive joint diseases.

Original languageEnglish (US)
Pages (from-to)196-201
Number of pages6
JournalCurrent Osteoporosis Reports
Volume9
Issue number4
DOIs
StatePublished - Dec 2011
Externally publishedYes

Fingerprint

Chondrocytes
Joints
Articular Cartilage
Osteoarthritis
Advanced Glycosylation End Products
Joint Diseases
Reactive Oxygen Species
Cytokines
Phenotype
Enzymes
Proteins
Therapeutics

Keywords

  • Aging
  • Chondrocytes
  • Osteoarthritis
  • Senescence

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism

Cite this

Events in articular chondrocytes with aging. / Leong, Daniel J.; Sun, Hui (Herb).

In: Current Osteoporosis Reports, Vol. 9, No. 4, 12.2011, p. 196-201.

Research output: Contribution to journalArticle

Leong, Daniel J. ; Sun, Hui (Herb). / Events in articular chondrocytes with aging. In: Current Osteoporosis Reports. 2011 ; Vol. 9, No. 4. pp. 196-201.
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