SCARF1, also known as scavenger receptor class F member 1, SREC-1 or SR-F1, is a type I transmembrane protein belonging to the scavenger receptor superfamily. It plays a key role in the binding and endocytosis of various endogenous and exogenous ligands, and is essential for maintaining homeostasis and immunity. It is involved in multiple biological processes including innate and adaptive immunity, and its associated pathways may include those related to ligand recognition and immune response regulation [1,2]. Genetic models, such as gene-knockout mouse models, have been valuable in studying SCARF1.

SCARF1-deficient mice develop a severe resting phenotype with a systemic lupus erythematosus (SLE)-like disease, highlighting its importance in the clearance of apoptotic host cells in maintaining homeostasis [1,5]. In liver transplantation models, overexpression of SCARF1 in Kupffer cells improves acute rejection and liver function, as it promotes M2 polarization of Kupffer cells through the calcium-dependent PI3K-AKT-STAT3 signalling pathway [3]. In hepatocellular carcinoma, SCARF1 expression is downregulated in tumor tissues, and higher expression is prognostic of better survival, with SCARF1 playing a role in the recruitment of pro-inflammatory CD4+ T cells [4].

In conclusion, SCARF1 is crucial for maintaining homeostasis, especially in the clearance of apoptotic cells. Its deficiency leads to the development of SLE-like diseases in mice. In addition, it plays important roles in liver transplantation and hepatocellular carcinoma, as revealed through model-based research. The study of SCARF1 using KO mouse models has provided valuable insights into its functions in these specific disease areas.