Tao Haolin, Mo Yingshi, Liu Wenbin, Wang Hui
College of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou 510006, China.
Guangdong Provincial Key Laboratory of Pharmaceutical Bioactive Substances, Guangdong Pharmaceutical University, Guangzhou 510006, China.
Int Immunopharmacol. 2023 Apr;117:109977. doi: 10.1016/j.intimp.2023.109977. Epub 2023 Mar 9.
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.
痛风是一种由单钠尿酸盐（MSU）晶体在关节内沉积引起的代谢性疾病，可导致炎症和组织损伤。血清尿酸浓度升高是痛风发展的关键步骤。血清尿酸由肾脏和肠道中的尿酸转运蛋白调节，尤其是葡萄糖转运蛋白9（GLUT9，SLC2A9）、尿酸盐转运蛋白1（URAT1，SLC22A12）和ATP结合盒转运体G（ABCG）。单钠尿酸盐晶体激活NLRP3炎性小体并随后释放白细胞介素-1β，引发急性痛风性关节炎的加重，而中性粒细胞胞外陷阱（NETs）被认为在数天内推动痛风的自行缓解。若不治疗，急性痛风最终可能发展为慢性痛风石性痛风，其特征为痛风石、慢性痛风性滑膜炎和关节结构损伤，带来沉重的治疗负担。尽管近年来对痛风病理机制的研究逐渐深入，但痛风的许多临床表现仍无法得到充分阐释。在此，我们综述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提供帮助。
