Panx1, or pannexin 1, is an ubiquitously expressed protein that forms an ATP-releasing membrane channel. It is involved in multiple biological processes, including inflammation, blood pressure regulation, and is associated with pathways like Akt-FOXO1 and purinergic signaling. Its function is crucial in maintaining various physiological and pathophysiological processes [1,2,3]. Genetic models, such as knockout (KO) and conditional knockout (CKO) mouse models, have been valuable in studying Panx1.

In cardiomyocytes, Panx1 deletion in Panx1MyHC6 mice increased glycolytic metabolism and protected against cardiac hypertrophy in non-ischemic heart failure, potentially by reducing immune cell recruitment [1]. In the liver, global or hepatic Panx1 knockdown in mice disturbed glucolipid metabolism, while its overexpression ameliorated the dysregulation, with Panx1-mediated ATP release playing a crucial role in maintaining hepatic glucolipid homeostasis [2]. In the brain, PANX1-/-mice showed capillary dilation, blood flow increase, and impaired vasodilation, indicating that purines released through PANX1 channels play important roles in regulating neurovascular structure and function [3]. In a pain model, global or neuron-specific Panx1 deletion in mice decreased pain thresholds after complete Freund's adjuvant stimuli, revealing Panx1's positive correlation with pain sensitivity [4].

In conclusion, Panx1 is essential for maintaining normal physiological functions in various tissues. KO/CKO mouse models have revealed its roles in diseases such as heart failure, disorders of glucolipid metabolism, neurovascular dysfunctions, and inflammatory pain, providing potential therapeutic targets for these disease areas.