Aoc3, also known as semicarbazide-sensitive amine oxidase and vascular adhesion protein 1 (VAP1), is a membrane-bound adhesion protein. It facilitates leukocyte-endothelial cell adhesion, and its enzymatic function involves catalyzing the oxidative deamination of primary amines to generate hydrogen peroxide (H2O2). It is associated with inflammation-related pathways and plays important roles in various biological processes and diseases [1,4].

Aoc3 deficiency in mice has shown several impacts. In ApoE-/-Aoc3-/-mice, atherosclerotic plaques increased at an early stage, related to VSMC dedifferentiation and higher T-cell recruitment in plaques due to MCP-1 augmentation [2]. Aoc3 knockout mice were more prone to DSS-induced colitis and colonic tumorigenesis, with shorter survival in colitis models and more tumors in both AOM/DSS and Apc mutant mice models [3]. In the context of myocardial infarction, Aoc3 knockdown alleviated cardiac fibrosis and improved cardiac function and hypertrophy in mice [4].

In conclusion, Aoc3 is crucial in processes like inflammation, leukocyte adhesion, and oxidative stress generation. Gene knockout mouse models have revealed its role in diseases such as atherosclerosis, colitis, colonic tumorigenesis, and cardiac remodelling after myocardial infarction, providing insights into potential therapeutic targets for these diseases.