The Age-Related Changes in Cartilage and Osteoarthritis

被引:138
|
作者
Li, YongPing [1 ]
Wei, XiaoChun [1 ]
Zhou, JingMing [2 ]
Wei, Lei [1 ,2 ]
机构
[1] Shanxi Med Univ, Hosp 2, Dept Orthopaed, Taiyuan 030001, Shanxi, Peoples R China
[2] Brown Univ, Rhode Isl Hosp, Dept Orthopaed, Warren Alpert Med Sch, Providence, RI 02903 USA
关键词
HUMAN ARTICULAR-CARTILAGE; GLYCATION END-PRODUCTS; CHROMATIN PROTEIN HMGB2; FACTOR RECEPTOR 1; GROWTH-FACTOR-I; TGF-BETA; CHONDROCYTE SENESCENCE; OXIDATIVE STRESS; DOWN-REGULATION; CELL-DEATH;
D O I
10.1155/2013/916530
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Osteoarthritis (OA) is closely associated with aging, but its underlying mechanism is unclear. Recent publications were reviewed to elucidate the connection between aging and OA. With increasing OA incidence, more senior people are facing heavy financial and social burdens. Age-related OA pathogenesis is not well understood. Recently, it has been realized that age-related changes in other tissues besides articular cartilage may also contribute to OA development. Many factors including senescence-related secretory phenotypes, chondrocytes' low reactivity to growth factors, mitochondrial dysfunction and oxidative stress, and abnormal accumulation of advanced glycation end products (AGEs) may all play key roles in the pathogenesis of age-related OA. Lately, epigenetic regulation of gene expression was recognized for its impact on age-related OA pathogenesis. Up to now, few studies have been reported about the role of miRNA and long-noncoding RNA (lncRNA) in age-related OA. Research focusing on this area may provide valuable insights into OA pathogenesis. OA-induced financial and social burdens have become an increasingly severe threat to older population. Age-related changes in noncartilage tissue should be incorporated in the understanding of OA development. Growing attention on oxidative stress and epigenetics will provide more important clues for the better understanding of the age-related OA.
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收藏
页数:12
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