Lxn, also known as latexin, is a gene with diverse functions. It acts as a carboxypeptidase inhibitor and is involved in multiple biological processes. Lxn plays a role in regulating the cytoskeleton in vascular endothelial cells, hematopoiesis, and is associated with various signaling pathways such as JAK1/STAT3 in macrophages [1,2,3]. It has implications in maintaining vascular homeostasis, immune regulation, and stem cell-related processes, making it an important target for understanding disease mechanisms [1,2,3].

In gene knockout studies, Lxn deficiency in mice leads to several significant outcomes. In vascular endothelial cells, it promotes proteolytic cleavage of Filamin A, regulating cytoskeleton remodelling, which improves vascular permeability, vasodilation, and atherosclerosis [1]. In macrophages, it promotes M2 polarization and PD-L2 expression, contributing to cancer immune-escape [2]. In the context of atherosclerosis, Lxn deletion limits foam cell formation and ameliorates the disease by promoting macrophage phenotype differentiation [4]. In the intestine, Lxn deficiency promotes the proliferation of intestinal stem cells, enhancing intestinal organogenesis and injury repair [5].

In conclusion, Lxn has essential functions in maintaining the normal physiological state of multiple tissues and organs. Gene knockout mouse models have revealed its role in diseases such as atherosclerosis, cancer, and intestinal injury-related conditions. Understanding Lxn's functions provides potential new strategies for the treatment of these diseases.