Abstract
Acid-sensing ion channel 1a (ASIC1a) is a member of the extracellular H+-activated cation channel family. Emerging evidence has suggested that ASIC1a plays a crucial role in the pathogenesis of rheumatoid arthritis (RA). Specifically, ASIC1a could promote inflammation, synovial hyperplasia, articular cartilage, and bone destruction; these lead to the progression of RA, a chronic autoimmune disease characterized by chronic synovial inflammation and extra-articular lesions. In this review, we provided a brief overview of the molecular properties of ASIC1a, including the basic biological characteristics, tissue and cell distribution, channel blocker, and factors influencing the expression and function, and focused on the potential therapeutic targets of ASIC1a in RA and possible mechanisms of blocking ASIC1a to improve RA symptoms, such as regulation of apoptosis, autophagy, pyroptosis, and necroptosis of articular cartilage, and synovial inflammation and invasion of fibroblast-like cells in synovial tissue.
Highlights
As a chronic systemic autoimmune disease, the main pathological characteristics of rheumatoid arthritis (RA) include synovial cell proliferation, multiple inflammatory cell infiltration, pannus formation, and cartilage and bone tissue destruction, which thereby eventually lead to joint deformity and loss of function [1]
Our previous studies have demonstrated that ASIC1a is involved in the injury of articular chondrocytes that is caused by increased intracellular calcium ([Ca2+]i) induced by extracellular acidification; this can be significantly attenuated by the use of amiloride and the ASIC1a-specific blocker psalmotoxin 1 (PCTX-1) [15,16,17]
We found that ASIC1a, ASIC2a, and ASIC3 were expressed in the articular chondrocytes of rats with adjuvant arthritis (AA), and that the expression levels of ASIC1awere significantly higher than those of other subunits [4]
Summary
As a chronic systemic autoimmune disease, the main pathological characteristics of rheumatoid arthritis (RA) include synovial cell proliferation, multiple inflammatory cell infiltration, pannus formation, and cartilage and bone tissue destruction, which thereby eventually lead to joint deformity and loss of function [1]. Numerous studies have demonstrated that synovial inflammation and extracellular acidification play an important role in the occurrence and development of the RAmediated destruction of articular cartilage and bone [3, 4].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
