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 binding and acts as an ectoenzyme catalyzing primary amine oxidative deamination, generating hydrogen peroxide. Aoc3 is involved in inflammation-related pathways and has significance in various biological processes and disease conditions. Genetic models, like knockout mice, are valuable for studying its functions [1,2,5].

Aoc3 deficiency in mice led to increased susceptibility to DSS-induced colitis and colonic tumorigenesis, with Aoc3 knockout mice showing more tumors in AOM/DSS and Apc mutant mice models [4]. In ApoE-/-Aoc3-/-mice, Aoc3 knockout increased atherosclerotic plaques at an early stage, related to VSMC dedifferentiation and higher T-cell recruitment [3]. Also, Aoc3 knockdown in mice alleviated cardiac fibrosis after myocardial infarction, improving cardiac function and hypertrophy [5].

In conclusion, Aoc3 plays crucial roles in inflammation, cell-cell adhesion, and oxidative stress-related biological processes. Mouse knockout models have revealed its significance in diseases such as colitis, colonic tumorigenesis, atherosclerosis, and cardiac remodelling after myocardial infarction, providing insights for potential therapeutic targeting.