Ilf3, also known as Interleukin enhancer-binding factor 3, is a gene with diverse functions. It encodes double-stranded RNA-binding proteins that are involved in multiple RNA metabolism processes. Ilf3 is implicated in regulating the cell cycle, enzymatic activities, and is associated with pathways like mTORC1-dependent amino acid sensing, innate immune response, and serine biosynthesis [1,3,4].

Macrophage-conditional Ilf3 knockout (Ilf3M-KO) and transgenic (Ilf3M-Tg) mice, as well as smooth muscle-conditional Ilf3 knockout (Ilf3SM-KO) and transgenic (Ilf3SM-Tg) mice, have been used to study its functions. In macrophages, Ilf3 deficiency attenuates abdominal aortic aneurysm progression, while its elevation exacerbates the lesions. Mechanistically, it increases NF-κB activity and represses the anti-inflammatory action [2]. In atherosclerotic calcification, hyperlipidemia increases Ilf3 expression, and its deletion in relevant cell types may prevent and reverse the process by regulating BMP2 and STAT1 transcription [5].

In conclusion, Ilf3 plays crucial roles in multiple biological processes and disease conditions. The use of Ilf3 KO/CKO mouse models has revealed its significance in abdominal aortic aneurysm development and atherosclerotic calcification, providing potential therapeutic targets for these diseases.