Arg1, also known as arginase 1, is an enzyme that catalyzes the hydrolysis of L-arginine to L-ornithine and urea, regulating the last step of the urea cycle. It is involved in multiple biological processes, such as immune response regulation, cell metabolism, and tissue repair [2,3,5]. Genetic models, especially KO mouse models, have been crucial for studying its functions.

In stroke mouse models, STAT6 deficiency led to reduced Arg1 expression in microglia/macrophages, impairing efferocytosis, increasing inflammation, and exacerbating infarct volume and long-term functional deficits, suggesting that STAT6/Arg1 signaling promotes inflammation resolution and improves stroke outcomes [1]. In cancer, in a mouse model of endometrial cancer, high ARG1 expression was associated with poor prognosis [3,5]. In breast cancer cells, overexpression of ARG1 suppressed cell proliferation, migration, and xenograft tumor growth by down-regulating p-AKT and de-activating the AKT signal pathway [4]. In lung fibrosis, macrophage-fibroblast crosstalk induced Arg1 expression in macrophages, which contributed to fibrotic responses by metabolizing arginine to ornithine for fibroblast collagen synthesis [6]. Also, selective depletion of Arg1-expressing tumor-associated macrophages in a tumor model inhibited tumor growth and reduced the ratio of TH1-Treg cells in the tumor microenvironment [7].

In conclusion, Arg1 plays essential roles in various biological processes and disease conditions. Studies using KO mouse models have revealed its significance in stroke, cancer, and lung fibrosis. Understanding Arg1's functions can provide insights into disease mechanisms and potential therapeutic targets in these disease areas.