Abstract：
Gout is a metabolic disease caused by the deposition of monosodium urate (MSU) crystals inside joints, which leads to inflammation and tissue damage. Increased concentration of serum urate is an essential step in the development of gout. Serum urate is regulated by urate transporters in the kidney and intestine, especially GLUT9 (SLC2A9), URAT1 (SLC22A12) and ABCG. Activation of NLRP3 inflammasome bodies and subsequent release of IL-1β by monosodium urate crystals induce the crescendo of acute gouty arthritis, while neutrophil extracellular traps (NETs) are considered to drive the self-resolving of gout within a few days. If untreated, acute gout may eventually develop into chronic tophaceous gout characterized by tophi, chronic gouty synovitis, and structural joint damage, leading the crushing burden of treatment. Although the research on the pathological mechanism of gout has been gradually deepened in recent years, many clinical manifestations of gout are still unable to be fully elucidated. Here, we reviewed the molecular pathological mechanism behind various clinical manifestations of gout, with a view to making contributions to further understanding and treatment.
摘要：
痛风是由尿酸单钠（MSU）晶体在关节内沉积引起的代谢性疾病，导致炎症和组织损伤.血清尿酸浓度的增加是痛风发展的重要步骤。血清尿酸受肾脏和肠道中尿酸转运蛋白的调节，特别是GLUT9（SLC2A9），URAT1（SLC22A12）和ABCG。NLRP3炎性体的激活和随后通过尿酸单钠晶体释放IL-1β诱导急性痛风性关节炎的渐增,而中性粒细胞胞外陷阱（NETs）被认为在几天内驱动痛风的自我解决。如果未经治疗,急性痛风最终可能发展为以痛风石为特征的慢性痛风石，慢性痛风性滑膜炎,和结构接缝损坏，导致处理的破碎负担。虽然近年来对痛风病理机制的研究逐渐深入,痛风的许多临床表现仍无法完全阐明。这里,我们回顾了痛风各种临床表现背后的分子病理机制，以期为进一步的理解和治疗作出贡献。
