Fabp4, also known as fatty acid binding protein 4 or aP2, is a cytoplasmic fatty acid chaperone. It is highly expressed in adipose tissue and myeloid cells, functioning as a lipid chaperone protein and playing a role in lipid metabolism. It impacts cells through JAK2/STAT2 and c-kit pathways, and is involved in processes like angiogenesis, vascular smooth muscle cell proliferation and migration. Additionally, it is a secreted hormone maintaining glucose homeostasis [2,5,6].

In ovarian cancer cells, knockdown of FABP4 led to increased 5-hydroxymethylcytosine levels in the DNA, downregulation of metastasis-associated gene signatures, and reduced clonogenic cell survival. CRISPR-mediated knockout in high-grade serous ovarian cancer cells decreased metastatic tumor burden in mice [1]. In elderly mice, silencing FABP4 rejuvenated aging-associated decline in metabolic activities, reversing metabolic disorders by promoting cholesterol and fatty acid degradation and suppressing gluconeogenesis [3]. In TNBC, knocking down Fabp4 or inhibiting its activity suppressed tumor progression in mouse models [4].

In conclusion, Fabp4 is crucial in lipid metabolism and glucose homeostasis. Gene-knockout models in mice have revealed its role in various disease conditions such as ovarian cancer metastasis, aging-associated metabolic disorders, and TNBC progression. These findings highlight its potential as a therapeutic target in these disease areas.