Osteoarthritis: Aging of matrix and cells - Going for a remedy

被引:57
作者
Aigner, T.
Haag, J.
Martin, J.
Buckwalter, J.
机构
[1] Univ Leipzig, Inst Pathol, D-04301 Leipzig, Germany
[2] Univ Iowa, Coll Med, Dept Orthopaed, Iowa City, IA 52242 USA
关键词
senescence; galactosidase; DNA damage; glycation;
D O I
10.2174/138945007779940070
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
It has been known for a very long time that aging is the most prominent risk factor for the initiation and progression of osteoarthritis. This might be related to continuous mechanical wear and tear and/or result from time/age-related modifications of cartilage matrix components. Also a mere loss of viable cells over time, due to apoptosis or any other mechanism, might contribute. More recent evidence, however, supports that stressful conditions for the cells might promote chondrocyte senescence and might be in particular important for the progression of the osteoarthritic disease process. One of the most important implications of this hypothesis is that it points to issues of cellular degeneration as the basis for understanding of the initiation and the progression of osteoarthritis. Equally important, it emphasizes that whatever treatment we envisage for osteoarthritis, we must take into account that we are dealing with aged/(pre) senescent cells which no longer have the abilities of their juvenile counterparts to respond to the many mechanical, inflammatory, and traumatic assaults to the tissue. Thirdly, this directs treatment options to deal with the senescence of cells, which are only conceptually available today.
引用
收藏
页码:325 / 331
页数:7
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