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Chondrocyte senescence and osteoarthritis : role of oxidized LDL-induced oxidative stress
https://kindai.repo.nii.ac.jp/records/10507
https://kindai.repo.nii.ac.jp/records/10507b73fd22f-95d0-4aaa-b211-e53776879aae
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AA0050842X-20100600-0001.pdf (3.8 MB)
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||
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| 公開日 | 2010-07-22 | |||||||||
| タイトル | ||||||||||
| タイトル | Chondrocyte senescence and osteoarthritis : role of oxidized LDL-induced oxidative stress | |||||||||
| 言語 | en | |||||||||
| 著者 |
Akagi, Masao
× Akagi, Masao
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| 言語 | ||||||||||
| 言語 | eng | |||||||||
| キーワード | ||||||||||
| 主題 | osteoarthritis, chondrocyte senescence, oxidative stress, oxidized LDL, LOX-1 | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | departmental bulletin paper | |||||||||
| 著者所属(翻訳) | ||||||||||
| 値 | Department of Orthopaedic Surgery, Kinki University Faculty of Medicine | |||||||||
| 版 | ||||||||||
| 出版タイプ | NA | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_be7fb7dd8ff6fe43 | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | The Kinki University Medical Association | |||||||||
| 書誌情報 |
en : ACTA MEDICA KINKI UNIVERSITY 巻 35, 号 1, p. 1-13, 発行日 2010-06-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 03866092 | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Although epidemiologic studies have shown that age is the chief risk factor for osteoarthritis (OA), the relationship between aging and the development of OA has not been completely understood yet. However, accumulating evidences in vivo and vitro have shown that the development of OA is, at least in part, attributable to the age-related chondrocyte senescence. This review focuses on how chondrocyte senescence affects the articular cartilage degeneration and how oxidative stress affects the chondrocyte senescence. Further, I would like to introduce our hypothesis that oxidized low-density lipoprotein, which is the most important molecule causing atherosclerosis, is involved in the pathogenesis of OA by playing a role as an oxidative stressor. It is interesting that even though mitotically inactive, senescent cells are far from being biologically inert. Many genes in senescent cells display higher expression levels that do not merely correlate with cell cycle arrest. Chondrocyte senescence is associated with an increased production of inflammatory mediators and matrix degrading enzymes characteristic of the senescent secretory phenotype. Age-related oxidative stress and damage may play a central role in cartilage aging through modulation of cell signaling pathways that regulate anabolic and catabolic activity. | |||||||||
| フォーマット | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | application/pdf | |||||||||
