Aqp1, a member of the aquaporin family of water channel proteins, contains two NPA motifs and is present in almost all organs and tissues. It is mainly responsible for water molecule transport, and some studies also suggest its role in transporting small volatile solutes like CO2 [2,5]. Aqp1 is involved in multiple biological processes, with its functions being crucial for maintaining normal physiological states.

In endothelial cells, disruption of Aqp1 leads to morphological and mitochondrial changes, senescence, and impaired angiogenesis, while knockdown or blockade in senescent endothelial cells rescues the excess H2O2-induced senescence phenotype and metabolic dysfunction, highlighting its role in regulating endothelial cell senescence and angiogenesis [1]. In peritoneal dialysis patients, a common Aqp1 promoter variant rs2075574 is associated with decreased ultrafiltration and an increased risk of death or technique failure, and Aqp1-containing exosomes in peritoneal dialysis effluent may serve as a biomarker of dialysis efficiency [3,4]. Additionally, Aqp1 suppression by ATF4 triggers trabecular meshwork tissue remodelling in ET-1-induced primary open-angle glaucoma [6].

In summary, Aqp1 plays essential roles in processes such as endothelial cell senescence, peritoneal dialysis-related water transport, and trabecular meshwork tissue remodelling in glaucoma. The use of genetic models, like potential Aqp1 KO or CKO mouse models (although not explicitly detailed in these references), could further deepen our understanding of its functions in these disease-related contexts, contributing to the exploration of new therapeutic strategies for age-related cardiovascular diseases, peritoneal dialysis-associated complications, and primary open-angle glaucoma.