Litaf, also known as lipopolysaccharide-induced tumor necrosis factor-α factor or p53-induced gene 7 (PIG7), is a protein with diverse functions. It acts as a transcription factor that can activate the transcription of TNF-α and is involved in regulating the inflammatory response. It also participates in various cellular processes such as membrane repair, ion channel regulation, and is associated with pathways like NF-κB, ASK1-JNK/p38, and FOXO1-SIRT1 [1,2,3]. It is of great biological importance as it is involved in multiple disease-related processes and cellular functions. Genetic models, especially gene knockout models, are valuable for studying its functions.

In gene knockout studies, LITAF deficiency exacerbated cardiac hypertrophy and fibrosis compared with wild-type mice, indicating its role as a negative regulator of cardiac remodeling [2]. In atherosclerotic plaque formation, the area of atherosclerotic plaques was substantially lower in LITAF-/-mice compared to the control group, suggesting LITAF promotes atherosclerotic plaque formation through the NF-κB pathway [4].

In conclusion, Litaf plays essential roles in membrane repair, regulation of cardiac remodeling, and atherosclerotic plaque formation. Gene knockout mouse models have significantly contributed to understanding its functions in cardiac and atherosclerotic disease areas, providing insights into the underlying molecular mechanisms and potential therapeutic targets.