Osteoarthritis and nitric oxide
Osteoarthritis and nitric oxide
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DOI：
10.1016/s1063-4584(08)60008-4
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发表时间：
2008-06-01
影响因子：
7
通讯作者：
Abramson, Steven B.
中科院分区：
文献类型：
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作者：
Abramson, Steven B.
骨关节炎（OA）是由生物化学和机械因素引起的。虽然这种疾病的发病机制尚未完全了解，但研究人员已经确定了一些在疾病过程中起作用的分解代谢和保护因素。一氧化氮（NO）及其氧化还原衍生物似乎有许多不同的功能，在正常和病理生理关节条件。直到最近，NO被认为是一种分解代谢因子，其通过介导促炎细胞因子的表达、抑制胶原和蛋白聚糖的合成以及诱导细胞凋亡而负责使OA疾病过程永久化。然而，最近的研究表明，NO及其氧化还原衍生物也可能对软骨具有保护作用。本文综述了NO对软骨和软骨细胞的影响，并讨论了NO和/或其衍生物对其他细胞类型的潜在保护作用的一些证据。需要更多的研究来阐明NO及其衍生物对正常和骨关节炎软骨的作用。
Osteoarthritis (OA) is caused by both biochemical and mechanical factors. While the mechanisms that underlie the disease are not completely understood, investigators have characterized a number of catabolic and protective factors that have a role in the disease process. Nitric oxide (NO) and its redox derivatives appear to have a number of different functions in both normal and pathophysiological joint conditions. Until recently, NO was considered a catabolic factor that was responsible for perpetuating the OA disease process by mediating the expression of proinflammatory cytokines, inhibiting the synthesis of collagen and proteoglycans and inducing apoptosis. However, recent studies suggest that NO and its redox derivatives may also have protective effects on cartilage. This review will summarize the literature on the effects of NO on cartilage and chondrocytes as well as discuss some evidence that suggests potential protective effects of NO and/or its derivatives on other cell types. More research is needed to elucidate the role of NO and its derivatives on both normal and osteoarthritis cartilage.