The development from hyperuricemia to gout: key mechanisms and natural products for treatment

Lin Liu, Dan Wang, Mengyang Liu, Haiyang Yu, Qian Chen, Yuzheng Wu, Ruixia Bao, Y. Zhang, Tao Wang
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引用次数: 12

Abstract

Abstract Gout is a common of inflammatory arthritis and is caused by the deposition of monosodium urate (MSU) crystals as a result of hyperuricemia (HUA). Although HUA is considered to be the main risk factor for gout, only approximately 10% of the individuals with HUA will eventually experience a gout attack. In this review, we first briefly introduce the development of gout and then summarize several possible reasons for its development. Genetic factors play a more prominent role in gout than in other diseases; functional mutations related to urate control and innate immunity components have been found to be associated with gout. Here, we list some of the most prominent genes involved in the pathogenesis of gout. In joints with MSU deposition, mature macrophages may uptake MSU crystals without causing inflammation, and this helps to maintain joints in an asymptomatic state. As an auxiliary inflammation pathway, the ATP-P2X7R-NLRP3 axis may contribute to the amplification of MSU-induced inflammation to affect the development of gout. Finally, this review summarizes the research progress on natural products that can be used in the treatment of HUA and gout.
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从高尿酸血症到痛风的发展:关键机制和治疗的天然产物
痛风是一种常见的炎性关节炎,是由高尿酸血症(HUA)引起的尿酸钠(MSU)晶体沉积引起的。虽然HUA被认为是痛风的主要危险因素,但只有大约10%的HUA患者最终会经历痛风发作。在本文中,我们首先简要介绍了痛风的发展,然后总结了其发展的几种可能原因。遗传因素在痛风中的作用比其他疾病更突出;与尿酸控制和先天免疫成分相关的功能突变已被发现与痛风有关。在这里,我们列出了一些最突出的基因参与发病机制的痛风。在MSU沉积的关节中,成熟的巨噬细胞可以摄取MSU晶体而不引起炎症,这有助于维持关节处于无症状状态。作为一种辅助炎症通路,ATP-P2X7R-NLRP3轴可能参与msu诱导炎症的扩增,从而影响痛风的发生。最后,综述了用于HUA和痛风治疗的天然产物的研究进展。
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