Peroxidasin (PXDN), also known as Vascular Peroxidase-1 (VPO1), is a heme-containing peroxidase. It catalyzes the oxidation of various substrates using hydrogen peroxide (H2O2), playing diverse roles in physiology and pathology. It is involved in innate immunity, cardiovascular physiology and diseases, extracellular matrix formation, and has been associated with pathways like autophagy, oxidative stress, and inflammation [1]. Genetic models, such as gene knockout mice, are valuable for studying its functions.

In mice, biallelic deletion of Pxdn using the CRISPR/Cas9 system led to anophthalmia and severe eye malformation, indicating PXDN's essential role in eye development. Homozygous mice showed extreme eye-development defects, while heterozygous mice had normal eye structure and function, suggesting a single allele of the Pxdn gene suffices for normal eye-structure formation and visual function [3]. In addition, in an elastase-induced mouse abdominal aortic aneurysm (AAA) model, alpha-ketoglutarate (AKG) treatment suppressed the development of AAA by inhibiting the PXDN/HOCL/ERK signaling pathways [2].

In conclusion, PXDN is crucial for multiple biological processes. Its role in eye development is clearly demonstrated through Pxdn knockout mouse models. In disease areas, the study of PXDN in mouse models provides insights into conditions like abdominal aortic aneurysm, highlighting its potential as a therapeutic target.