Serpina3n, a secretory serine protease inhibitor belonging to clade "a", exhibits unique structural and physiological characteristics. It plays significant roles in various biological processes such as the complement cascade, apoptosis, and wound healing by inhibiting a wide range of proteases [2]. Clinically, its human orthologue SERPINA3 is dysregulated in brain cells, cerebrospinal fluid, and plasma in various neurological conditions [1].

In a Serpina3n conditional knockout mice model, genetic deletion of SerpinA3n led to increased activity of substrate proteases, poorly compacted matrix, and significantly worse post-infarct cardiac function. This demonstrated a causal role of Serpins in regulating matrix function and post-infarct cardiac remodelling [3]. In another study, hepatic deletion of SerpinA3N in male mice attenuated steatosis, correlated with altered lipid metabolism genes, increased fatty acid oxidation activity, and enhanced insulin signaling in mice with non-alcoholic fatty liver disease (NAFLD) [4].

In conclusion, Serpina3n is involved in multiple biological processes, and its functions are further elucidated through gene knockout mouse models. These models have revealed its roles in cardiac remodelling after myocardial infarction and in regulating NAFLD and glucose homeostasis, providing insights into potential therapeutic strategies for related diseases.