a Department of Rheumatology , The Affiliated Hospital to Changchun University of Chinese Medicine , Changchun , PR China.
b Department of Emergency , The First Hospital of Jilin University , Changchun , PR China.
Immunopharmacol Immunotoxicol. 2018 Aug;40(4):273-277. doi: 10.1080/08923973.2018.1485156. Epub 2018 Jul 23.
Acid-sensing ion channels (ASIC) are voltage-independent cationic channels that open in response to decrease in extracellular pH. Amongst different subtypes, ASIC3 has received much attention in joint inflammatory conditions including rheumatoid arthritis. There have been a number of studies showing that there is an increase in expression of ASIC3 on nerve afferents supplying joints in response to inflammatory stimulus. Accordingly, a number of selective as well as nonselective ASIC3 inhibitors have shown potential in attenuating pain and inflammation in animal models of rheumatoid arthritis. On the other hand, there have been studies showing that ASIC3 may exert protective effects in joint inflammation. ASIC animals, without ASIC3 genes, exhibit more joint inflammation and destruction in comparison to ASIC animals. The present review discusses the dual nature of ASIC3 in joint inflammation with possible mechanisms.
酸敏离子通道（ASIC）是一种电压不依赖性阳离子通道，在细胞外 pH 值降低时开放。在不同的亚型中，ASIC3 在包括类风湿关节炎在内的关节炎症性疾病中受到了广泛关注。有许多研究表明，在炎症刺激下，供应关节的神经传入纤维上 ASIC3 的表达增加。因此，一些选择性和非选择性的 ASIC3 抑制剂在类风湿关节炎的动物模型中显示出了减轻疼痛和炎症的潜力。另一方面，也有研究表明 ASIC3 可能在关节炎症中发挥保护作用。与 ASIC 动物相比，缺乏 ASIC3 基因的 ASIC 动物在关节炎症和破坏方面表现出更多的炎症和破坏。本综述讨论了 ASIC3 在关节炎症中的双重性质及其可能的机制。
