P2rx1, a member of the purinergic receptor family, plays significant roles in various biological processes. It is involved in purinergic signaling, which is crucial in initiating and amplifying inflammatory signals [4]. P2rx1 has been linked to multiple pathways including those related to mitochondrial dynamics, immune cell function, and innate immune-mediated inflammation [2,3].

Genetic knockout (KO) mouse models have provided valuable insights into the function of P2rx1. In pancreatic cancer liver metastasis, P2RX1-negative neutrophils accumulate and exhibit increased immunosuppressive molecules like PD-L1, with enhanced mitochondrial metabolism. The transcription factor Nrf2 is upregulated in these P2rx1-deficient neutrophils [1]. In renal ischemia/reperfusion injury, P2rx1 expression is upregulated, and its genetic knockout preserves mitochondrial dynamics and reduces the formation of neutrophil extracellular traps (NETs) [2]. P2rx1 knockout in mice also alleviates acetaminophen-induced acute liver failure by regulating the STING-TBK1-P65 signaling pathways [3]. In acute pancreatitis, genetic ablation of P2rx1 alleviates inflammatory responses as neutrophil-derived P2rx1 promotes neutrophil activation via glycolytic metabolism [4]. In colitis, genetic knockout of P2rx1 suppresses inflammation responses, inhibits neutrophil infiltration, and modulates the intestinal microbiota [5].

In conclusion, P2rx1 is involved in key biological processes such as inflammation regulation, immune cell function, and mitochondrial dynamics. KO mouse models have demonstrated its significance in diseases including pancreatic cancer, kidney injury, liver failure, acute pancreatitis, and colitis. Understanding P2rx1 function through these models offers potential therapeutic strategies for these disease conditions.