Osteoarthritis (OA) is a degenerative disease resulting from progressive joint destruction caused by many factors. Its pathogenesis is complex and has not been elucidated to date. Advanced glycation end products (AGEs) are a series of irreversible and stable macromolecular complexes formed by reducing sugar with protein, lipid, and nucleic acid through a non-enzymatic glycosylation reaction (Maillard reaction). They are an important indicator of the degree of ageing. Currently, it is considered that AGEs accumulation in vivo is a molecular basis of age-induced OA, and AGEs production and accumulation in vivo is one of the important reasons for the induction and acceleration of the pathological changes of OA. In recent years, it has been found that AGEs are involved in a variety of pathological processes of OA, including extracellular matrix degradation, chondrocyte apoptosis, and autophagy. Clearly, AGEs play an important role in regulating the expression of OA-related genes and maintaining the chondrocyte phenotype and the stability of the intra-articular environment. This article reviews the latest research results of AGEs in a variety of pathological processes of OA, to provide a new direction for the study of OA pathogenesis and a new target for prevention and treatment. Cite this article: Bone Joint Res 2022;11(5):292-300.

中文翻译：

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AGEs在骨关节炎软骨破坏发病机制中的作用。

骨关节炎（OA）是一种退行性疾病，由多种因素引起的进行性关节破坏引起。其发病机制复杂，迄今尚未阐明。高级糖基化终产物（AGEs）是由糖与蛋白质、脂质和核酸通过非酶促糖基化反应（美拉德反应）还原形成的一系列不可逆且稳定的大分子复合物。它们是老化程度的重要指标。目前认为，AGEs在体内的积累是老年性OA的分子基础，AGEs在体内的产生和积累是诱发和加速OA病理变化的重要原因之一。近年来发现AGEs参与了OA的多种病理过程，包括细胞外基质降解、软骨细胞凋亡和自噬。显然，AGEs在调节OA相关基因的表达、维持软骨细胞表型和关节内环境的稳定性方面发挥着重要作用。本文综述AGEs在OA多种病理过程中的最新研究成果，为OA发病机制研究提供新方向和防治新靶点。引用这篇文章：为OA发病机制研究提供新方向和防治新靶点。引用这篇文章：为OA发病机制研究提供新方向和防治新靶点。引用这篇文章：骨关节水库2022；11(5):292-300。