ASIC2, also known as acid-sensing ion channel 2, is a key molecule in various biological processes. It is involved in mechanosensation, with its role in the mechano-electrical transduction of arterial baroreceptors being notable. It interacts with other molecules like TRPV1, β-epithelial Na+ channel (βENaC), and PSD-95, participating in related pathways [1,2,7,8]. It has potential importance in the context of diseases such as pulmonary fibrosis, metabolic syndrome, and colorectal cancer [3,5,6].

In gene knockout studies, ASIC2-null mice have shown significant phenotypes. In renal afferent arterioles, the absence of ASIC2 (along with βENaC deficiency) abolishes pressure-induced constriction, and these mice have mild renal injury and increased mean arterial blood pressure, indicating its role in myogenic constriction and blood pressure regulation [2]. In the context of drugs of abuse, Asic2-/-mice show increased conditioned place preference to cocaine and morphine, suggesting its role in drug-reinforced behavior [4]. Mice lacking both ASIC2 and βENaC are protected from high-fat-diet-induced metabolic syndrome, with improvements in body weight, fat mass, blood glucose, and lipid profiles [5].

In conclusion, ASIC2 is crucial for mechanosensation and plays important roles in multiple disease-related processes such as renal function regulation, response to drugs of abuse, and metabolic syndrome. Gene knockout mouse models of ASIC2 have been instrumental in revealing these functions, providing valuable insights into the underlying mechanisms and potential therapeutic targets for related diseases.