Litaf, also known as lipopolysaccharide-induced tumor necrosis factor-α factor and p53-induced gene 7 (PIG7), is a transcription factor involved in multiple biological processes. It activates the transcription of TNF-α and pro-inflammatory cytokines, regulating the inflammatory response. It is also associated with pathways like the NF-κB inflammatory pathway, and plays a role in processes such as membrane repair, cardiac remodeling, and cell death regulation [1,2,3,4,5]. Genetic models, especially knockout models, are valuable for studying its functions.

In cardiac remodeling, LITAF knockout mice showed exacerbated cardiac hypertrophy and fibrosis compared to wild-type mice, indicating LITAF's role as a negative regulator of cardiac remodeling by disrupting ASK1 dimerization and blocking its activation [2]. In atherosclerosis, knockout of the LITAF gene in C57BL/6J mice led to a substantially lower area of atherosclerotic plaques, suggesting that LITAF promotes atherosclerotic plaque formation through the NF-κB pathway [4].

In conclusion, Litaf is a multi-functional gene involved in membrane repair, cardiac remodeling, and atherosclerotic plaque formation. Studies using gene knockout mouse models have revealed its role in these processes, contributing to our understanding of related disease mechanisms such as cardiac hypertrophy and atherosclerosis.