Fabp1, also known as liver-type fatty acid binding protein, plays a pivotal role in the metabolism of fatty acids. It is thought to be involved in facilitating the intracellular transport of fatty acids and related ligands to metabolic enzymes [3]. It is associated with pathways such as the PPAR-related pathways, influencing processes like fatty acid oxidation and lipid homeostasis [1,2,4].

In hepatocellular carcinoma (HCC), FABP1 was found to be overexpressed in tumor-associated macrophages (TAMs) of III-stage compared to II-stage HCC tissues. FABP1 deficiency in TAMs inhibited HCC progression in vitro, and in FABP1-/-mice, tumors showed attenuation, along with changes in the proportion of immune cell subtypes, indicating its role in creating an immunosuppressive environment in HCC [1]. In IgA nephropathy, downregulation of PPARα was shown to mediate FABP1 expression, affecting GPX4 and ACSL4 levels, causing ferroptosis in human mesangial cells and contributing to the pathogenesis [2]. In non-alcoholic steatohepatitis (NASH), intestinal PPARα signaling promotes NASH progression through regulating dietary fatty acid uptake via modulation of FABP1, as intestine-specific Ppara or Fabp1 disruption in mice fed a high-fat diet decreased obesity-associated metabolic disorders and NASH [4].

In conclusion, Fabp1 is essential for fatty acid metabolism and transport. Studies using gene-knockout mouse models have revealed its significant roles in multiple disease conditions including HCC, IgA nephropathy, and NASH. These models have provided insights into its functions in disease-related biological processes, highlighting its potential as a therapeutic target in these diseases.